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Background and Aims: While immune checkpoint inhibitors (ICIs) are revolutionising cancer therapy, checkpoint inhibitor-induced liver injury is a significant immune-related side effect of this immunotherapy. This study focuses on the severity classifications and characteristics of patients with checkpoint inhibitor-induced hepatitis., Methods: A retrospective analysis of patients with severe Checkpoint Inhibitor-induced hepatitis grade 3 and 4 according to the recommended Common Terminology Criteria for Adverse Events (CTCAE) classification was conducted. Data on clinicobiological characteristics, treatment and outcomes were collected from 3 university hospitals, and causality was assessed by using the updated Roussel Uclaf Causality Assessment Method. The severity of hepatitis was assessed using the Model for End-stage Liver Disease score, the Drug-Induced Liver Injury Network, and the Drug-Induced Liver Injury International Expert Working Group classifications., Results: We retrospectively included 100 patients presenting various hepatitis patterns with a median time to onset of 20 days after checkpoint inhibitors. Severity grading varied significantly among the classifications used. A lower incidence of severe cases was observed when using the Drug-Induced Liver Injury classifications instead of the recommended CCTCAE classification, and this was correlated with outcomes., Conclusions: This retrospective study challenges the efficacy of the CTCAE classification in defining the severity of Checkpoint Inhibitor-induced hepatitis and suggests that the traditional hepatology-focused scores may be more relevant. The CTCAE classification is inconsistent and gives equal weight to jaundice and elevated transaminases, which leads to steroid overtreatment and limits the rechallenge of ICIs., (© 2024 The Author(s). Alimentary Pharmacology & Therapeutics published by John Wiley & Sons Ltd.)

Background: Osimertinib, a third-generation EGFR tyrosine kinase inhibitor (TKI), demonstrated superior efficacy over first-generation TKIs in the FLAURA trial, resulting in its approval as first-line therapy for metastatic non-small-cell lung cancer (NSCLC). However, the real-world application of these trial results requires an evaluation of sequential therapeutic strategies. Methods: This retrospective, non-interventional study utilized data from the Epidemiological Strategy and Medical Economics (ESME) platform, which includes information on patients treated for lung cancer since 2015. Out of 39,974 patients in the database, 624 patients with EGFR -mutant advanced NSCLC treated with osimertinib as first-line (L1, n = 198) or second-line (L2, n = 426) treatment after first- or second-generation TKIs (n = 1262) were identified. Patient demographics, disease characteristics, treatment strategies, and disease progression were examined. Survival analyses were performed using Kaplan-Meier estimates and Cox proportional-hazards models. Results: In the study population (n = 624), 73.4% were female, with a median age of 70 years (range 28-93). Brain metastases at the start of osimertinib treatment were observed in 282 patients. ECOG PS-2 was reported in 29.4% of patients. The T790M mutation in exon 20 was identified in 257/426 patients (60.3%) receiving osimertinib in L2. Median progression-free survival (PFS) was 12.4 months (95% CI [10.7-14.7]) for L1 and 7.4 months (95% CI [6.2-8.7]) for L2. Median overall survival (OS) from advanced diagnosis was 28.5 months (95% CI [26.3-38.7]) for osimertinib L1 and 29.9 months (95% CI [28.6-31.8]) for osimertinib L2 (HR = 0.93; 95% CI [0.75-1.16]; p = 0.50). For L1, median OS was 27.1 months (95% CI [22.0-30.2]) for patients with cerebral metastases and 38.7 months (95% CI [26.3-52.8]) for those without (HR = 0.73; 95% CI [0.48-1.11]; p = 0.15). Discussion: Patients in the real-world ESME database exhibited a poorer prognosis compared to those in the FLAURA trial. The presence of cerebral metastases at diagnosis worsens the prognosis.

Introduction: In France, 40% of patients diagnosed with lung cancer are ≥70 years old, but these are under-represented in clinical trials. Using data from the French Epidemiological Strategy and Medical Economics (ESME) platform on Lung Cancer (LC), the objective is to provide an overview of the management and the prognosis of older patients with advanced or metastatic non-small cell lung cancer (AM-NSCLC) in a real-world context., Materials and Methods: From the ESME-LC database, we selected patients with AM-NSCLC (stage IIIB, IIIC, and IV), diagnosed between 2015 and 2019, and who received first-line systemic treatment. Demographics, tumour characteristics, and treatment received were described in patients ≥70, and compared to younger ones. Real-world progression-free survival (rwPFS) and overall survival (OS) were evaluated using the multivariable Cox model., Results: Among 10,002 patients with AM-NSCLC, the median age was 64 years, with 2,754 (27.5%) aged ≥70. In comparison with patients <70, older patients were more often male, with worse performance status and more comorbidities, but they were less underweight and more often non-smokers. The proportion of EGFR mutated non-squamous NSCLC was higher in older patients (25.0% vs 12.8%, p < 0.001), particularly among smokers and former smokers (12.7% vs 7.3%, p < 0.001). Among patients ≥70, 76.6% received first-line chemotherapy (including 67.0% treated with a platinum-based doublet), 15.0% received only targeted therapy, and 11.0% received immunotherapy (alone or in combination). Median first-line rwPFS was 5.1 months (95% confidence interval [CI] = [4.8;5.4]) for patients ≥70 and 4.6 months (95%CI = [4.4;4.8]) for patients <70, but age was not associated with rwPFS in multivariable analysis. Median OS was 14.8 months (95%CI = [13.9;16.1]) for patients ≥70 and 16.7 months (95%CI = [15.9;17.5]) for patients <70, with a significant effect of age in multivariable analysis for patients treated with chemotherapy and/or with targeted therapy, but not for patients treated with immunotherapy (alone or in combination with chemotherapy)., Discussion: In this real-world cohort of patients with AM-NSCLC, age was not associated with first-line rwPFS regardless of treatment received, nor with OS for patients receiving immunotherapy. However, OS was significantly shorter for patients aged ≥70 treated with chemotherapy or with targeted therapy alone., Competing Interests: Declaration of Competing Interest Mathilde Cabart reports non-financial support from Janssen, non-financial support from Pfizer, outside the submitted work. Loïc Mourey reports personal fees and non-financial support from Sanofi, personal fees from Astellas, personal fees and non-financial support from Janssen, personal fees and non-financial support from MSD, personal fees and non-financial support from BMS, personal fees and non-financial support from Ipsen, personal fees and non-financial support from Astra-Zeneca, personal fees and non-financial support from Pfizer, personal fees from Merck, outside the submitted work. David Pasquier has nothing to disclose. Sophie Schneider has nothing to disclose. Hervé Léna reports personal fees and non-financial support from Roche, personal fees from Astrazeneca, personal fees and non-financial support from MSD, personal fees and non-financial support from Novartis, personal fees and non-financial support from Takeda, personal fees from BMS, personal fees and non-financial support from Pfizer, non-financial support from Lilly, personal fees and non-financial support from Amgen, outside the submitted work. Nicolas Girard reports grants and personal fees from AstraZeneca, personal fees from Daiichi, grants and personal fees from Roche, grants and personal fees from MSD, grants and personal fees from BMS, grants and personal fees from Pfizer, grants and personal fees from Janssen, grants and personal fees from Boehringer Ingelheim, grants and personal fees from Takeda, grants and personal fees from Novartis, grants and personal fees from Sanofi, outside the submitted work; and Family Member employee of AstraZeneca. Christos Chouaid reports grants, personal fees and non-financial support from AstraZeneca, grants, personal fees and non-financial support from Boehringer Ingelheim, grants, personal fees and non-financial support from GSK, grants, personal fees and non-financial support from Roche, grants, personal fees and non-financial support from Sanofi Aventis, grants, personal fees and non-financial support from BMS, grants, personal fees and non-financial support from MSD, grants, personal fees and non-financial support from Lilly, grants, personal fees and non-financial support from Novartis, grants, personal fees and non-financial support from Pfizer, grants, personal fees and non-financial support from Takeda, grants, personal fees and non-financial support from Bayer, grants, personal fees and non-financial support from Janssen, grants, personal fees and non-financial support from Viatris, grants, personal fees and non-financial support from Chugai, grants, personal fees and non-financial support from Pierre Fabre, grants, personal fees and non-financial support from Amgen, outside the submitted work. Roland Schott reports personal fees and non-financial support from Roche, non-financial support from Takeda, personal fees and non-financial support from AstraZeneca, personal fees and non-financial support from Pfizer, non-financial support from IPSEN, personal fees and non-financial support from BMS, outside the submitted work. Sandrine Hiret reports non-financial support from Roche, non-financial support from Novartis, other from Sanofi, other from Astra Zeneca, other from Takeda, other from BMS, outside the submitted work. Didier Debieuvre has nothing to disclose. Xavier Quantin has nothing to disclose. Anne Madroszyk has nothing to disclose. Pascale Dubray-Longeras reports personal fees from MSD, personal fees from AstraZeneca, personal fees and non-financial support from Takeda, non-financial support from Pfizer, outside the submitted work. Eric Pichon reports personal fees and non-financial support from Takeda, personal fees from AstraZeneca, personal fees from MSD, outside the submitted work. Anne Baranzelli has nothing to disclose. Grégoire Justeau has nothing to disclose. Maurice Pérol reports personal fees and non-financial support from Takeda, personal fees from Janssen, personal fees and non-financial support from AstraZeneca, outside the submitted work. Lise Bosquet has nothing to disclose. Bastien Cabarrou has nothing to disclose., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Purpose: Although checkpoint inhibitors have improved first-line treatment for non-small cell lung cancer (NSCLC), a therapeutic need remains for patients whose disease does not respond or who experience disease progression after anti-PD-L1/PD-1 immunotherapy. CONTACT-01 (ClinicalTrials.gov identifier: NCT04471428) evaluated atezolizumab plus cabozantinib versus docetaxel in patients with metastatic NSCLC who developed disease progression after concurrent or sequential treatment with anti-PD-L1/PD-1 and platinum-containing chemotherapy., Methods: This multicenter, open-label, phase III trial randomly assigned patients 1:1 to atezolizumab 1,200 mg intravenously once every 3 weeks (q3w) plus cabozantinib 40 mg orally once daily or docetaxel 75 mg/m 2 intravenously once every 3 weeks. The primary end point was overall survival (OS)., Results: One hundred eighty-six patients were assigned atezolizumab plus cabozantinib, and 180 docetaxel. Minimum OS follow-up was 10.9 months. Median OS was 10.7 months (95% CI, 8.8 to 12.3) with atezolizumab plus cabozantinib and 10.5 months (95% CI, 8.6 to 13.0) with docetaxel (stratified hazard ratio [HR], 0.88 [95% CI, 0.68 to 1.16]; P = .3668). Median progression-free survival was 4.6 months (95% CI, 4.1 to 5.6) and 4.0 months (95% CI, 3.1 to 4.4), respectively (stratified HR, 0.74 [95% CI, 0.59 to 0.92]). Serious adverse events (AEs) occurred in 71 (38.4%) patients receiving atezolizumab plus cabozantinib and 58 (34.7%) receiving docetaxel. Grade 3/4 treatment-related AEs occurred in 73 (39.5%) patients receiving atezolizumab plus cabozantinib and 58 (34.7%) receiving docetaxel. Grade 5 AEs occurred in 14 (7.6%) and 10 (6.0%) patients in the atezolizumab plus cabozantinib and docetaxel arms, respectively (treatment-related in four [2.2%] and one [0.6%], respectively)., Conclusion: Atezolizumab plus cabozantinib after disease progression following anti-PD-L1/PD-1 immunotherapy and platinum-containing chemotherapy for metastatic NSCLC did not improve OS compared with docetaxel. Safety was consistent with known profiles of these agents.

Introduction: Lenvatinib plus pembrolizumab was found to have antitumor activity and acceptable safety in previously treated metastatic NSCLC. We evaluated first-line lenvatinib plus pembrolizumab versus placebo plus pembrolizumab in metastatic NSCLC in the LEAP-007 study (NCT03829332/NCT04676412)., Methods: Patients with previously untreated stage IV NSCLC with programmed cell death-ligand 1 tumor proportion score of at least 1% without targetable EGFR/ROS1/ALK aberrations were randomized 1:1 to lenvatinib 20 mg or placebo once daily; all patients received pembrolizumab 200 mg every 3 weeks for up to 35 cycles. Primary end points were progression-free survival (PFS) per Response Evaluation Criteria in Solid Tumors version 1.1 and overall survival (OS). We report results from a prespecified nonbinding futility analysis of OS performed at the fourth independent data and safety monitoring committee review (futility bound: one-sided p < 0.4960)., Results: A total of 623 patients were randomized. At median follow-up of 15.9 months, median (95% confidence interval [CI]) OS was 14.1 (11.4‒19.0) months in the lenvatinib plus pembrolizumab group versus 16.4 (12.6‒20.6) months in the placebo plus pembrolizumab group (hazard ratio = 1.10 [95% CI: 0.87‒1.39], p = 0.79744 [futility criterion met]). Median (95% CI) PFS was 6.6 (6.1‒8.2) months versus 4.2 (4.1‒6.2) months, respectively (hazard ratio = 0.78 [95% CI: 0.64‒0.95]). Grade 3 to 5 treatment-related adverse events occurred in 57.9% of patients (179 of 309) versus 24.4% (76 of 312). Per data and safety monitoring committee recommendation, the study was unblinded and lenvatinib and placebo were discontinued., Conclusions: Lenvatinib plus pembrolizumab did not have a favorable benefit‒risk profile versus placebo plus pembrolizumab. Pembrolizumab monotherapy remains an approved treatment option in many regions for first-line metastatic NSCLC with programmed cell death-ligand 1 tumor proportion score of at least 1% without EGFR/ALK alterations., Competing Interests: Disclosure Dr. Yang reports receiving funding to institution for serving on advisory or consultancy services for Daiichi Sankyo, Eli Lilly, Merck KGaA, Darmstadt, Germany, Merck Sharp & Dohme, Novartis, Roche, Genentech, Takeda Oncology, Yuhan Pharmaceuticals, Janssen Pharmaceuticals, Puma Technology, Gilead Sciences Inc., GlaxoSmithKline, BeiGene, Blueprint Medicines Corporation, Regeneron Pharmaceutical, and Taiho Pharmaceutical; receiving grant from Roche/Genentech; and having advisory or consultancy services from Ono Pharmaceuticals and Pfizer. Dr. Han reports receiving study funding to the institution from Eisai Inc., Nutley, New Jersey, and Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, to support study conduct. Dr. Jiménez reports receiving study funding to the institution from Eisai Inc., Nutley, New Jersey, and Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, to support study conduct. Dr. Lee reports receiving study funding to the institution from Eisai Inc., Nutley, New Jersey, and Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, to support study conduct. Dr. Koralewski reports receiving study funding to the institution from Eisai Inc., Nutley, New Jersey, and Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, to support study conduct. Dr. Karadurmus reports receiving study funding to the institution from Eisai Inc., Nutley, New Jersey, and Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, to support study conduct. Dr. Sugawara reports receiving grants or contracts to their institution from AnHeart, AstraZeneca, Chugai Pharma, MSD, Daiichi Sankyo, Bristol-Myers Squibb, Nippon Boehringer Ingelheim, Ono Pharmaceuticals, AbbVie, Amgen, Taiho Pharmaceutical, Takeda, and Clinipace; payment or honoraria from AstraZeneca, Chugai Pharma, Ono Pharmaceutical, Bristol-Myers Squibb, MSD, Nippon Boehringer Ingelheim, Pfizer, Taiho Pharmaceutical, Eli Lilly and Company, Novartis, Kyowa Kirin, Takeda, Nippon Kayaku, Merck Biopharma Japan, Amgen, AbbVie, Otsuka, Thermo Fisher Scientific, and Towa Pharmaceutical. Dr. Livi reports receiving study funding to the institution from Eisai Inc., Nutley, New Jersey, and Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, to support study conduct. Dr. Basappa reports receiving grants or contracts from Ipsen; receiving payment or honoraria from Bayer, Astellas, and Janssen; receiving support for attending meetings from Eisa, Ipsen, and Janssen; having participation on data safety monitoring board or advisory board with Eisai, Ipsen, Pfizer, Bristol-Myers Squibb, Roche, Janssen, AstraZeneca, EMD Serono, Bayer, Astellas, and MSD. Dr. Quantin reports receiving payment or honoraria to their institution from Sanofi, Bristol-Myers Squibb, and AstraZeneca; receiving support for attending meetings from Janssen Cilag, Sanofi, and Pfizer; and having participation on data safety monitoring board or advisory board with Bristol-Myers Squibb. Dr. Dudnik reports receiving study funding to the institution from Eisai Inc., Nutley, New Jersey, and Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, to support study conduct. Dr. Moran reports receiving support for present manuscript from MSD; grants or contracts from Abbott; consulting fees from Bristol-Myers Squibb and MSD; honoraria from Bristol-Myers Squibb, MSD, AstraZeneca, GlaxoSmithKline, Novartis, and Bayer; support for attending meetings from Tecnofarma, Roche, Pfizer, Bayer, and Janssen; and having participation on data safety monitoring board or advisory board with MSD. Dr. Mekhail reports receiving payment for speakers bureau from MSD. Drs. Okpara and Dutcus are employees of Eisai Ltd., Hatfield, UK. Drs. Zimmer, Samkari, and Bhagwati are employees of Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, and own stock in Merck & Co., Inc., Rahway, New Jersey. Dr. Csőszi reports receiving study funding to the institution from Eisai Inc., Nutley, New Jersey, and Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, to support study conduct., (Copyright © 2024 Merck Sharp & Dohme LLC., a subsidiary of Merck & Co., Inc., Rahway, NJ, USA, The Author(s). Published by Elsevier Inc. All rights reserved.)

Purpose: The RAS/MEK signaling pathway is essential in carcinogenesis and frequently altered in non-small-cell lung cancer (NSCLC), notably by KRAS mutations (KRASm) that affect 25%-30% of non-squamous NSCLC. This study aims to explore the impact of KRASm subtypes on disease phenotype and survival outcomes., Patients and Methods: We conducted a retrospective analysis of the French Epidemiological Strategy and Medical Economics database for advanced or metastatic lung cancer from 2011 to 2021. Patient demographics, histology, KRASm status, treatment strategies, and outcomes were assessed., Results: Of 10 177 assessable patients for KRAS status, 17.6% had KRAS p.G12C mutation, 22.6% had KRAS non-p.G12C mutation, and 59.8% were KRASwt. KRASm patients were more often smokers (96.3%) compared with KRASwt (85.8%). A higher proportion of programmed death-ligand 1 ≥50% was found for KRASm patients: 43.5% versus 38.0% (P < 0.01). KRASm correlated with poorer outcomes. First-line median progression-free survival was shorter in the KRASm than the KRASwt cohort: 4.0 months [95% confidence interval (CI) 3.7-4.3 months] versus 5.1 months (95% CI 4.8-5.3 months), P < 0.001. First-line overall survival was shorter for KRASm than KRASwt patients: 12.6 months (95% CI 11.6-13.6 months) versus 15.4 months (95% CI 14.6-16.2 months), P = 0.012. First-line chemoimmunotherapy offered better overall survival in KRAS p.G12C (48.8 months) compared with KRAS non-p.G12C (24.0 months) and KRASwt (22.5 months) patients. Second-line overall survival with immunotherapy was superior in the KRAS p.G12C subgroup: 12.6 months (95% CI 8.1-18.6 months) compared with 9.4 months (95% CI 8.0-11.4 months) for KRAS non-p.G12C and 9.6 months (8.4-11.0 months) for KRASwt patients., Conclusion: We highlighted distinct clinical profiles and survival outcomes according to KRASm subtypes. Notably KRAS p.G12C mutations may provide increased sensitivity to immunotherapy, suggesting potential therapeutic implications for sequencing or combination of therapies. Further research on the impact of emerging KRAS specific inhibitors are warranted in real-world cohorts., Competing Interests: Disclosure QDT received honoraria from Amgen, AstraZeneca, and Sanofi and meeting/travel support from Amgen and Sanofi. CC received grants or contracts, consulting fees, personal/institutional honoraria, and meeting/travel support from AstraZeneca, Amgen, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, GlaxoSmithKline, Lilly, Merck Sharp & Dohme (MSD), Novartis, Pfizer, Roche, Sanofi, and Takeda. TF received personal/institutional honoraria from Janssen, Lilly, and Roche. JRM received grants or contracts from MSD, received payment or honoraria for lectures, presentations, speaker’s bureaus, manuscript writing or educational events from AstraZeneca, Edimark, Janssen, MSD, Sanofi, Roche, and Takeda and meeting/travel support from Ose-Immunotherapeutics. MP received consulting fees from AstraZeneca, Bristol-Myers Squibb, Daiichi Sankyo, Eli Lilly, Eisai, GlaxoSmithKline, Ipsen, Janssen, MSD, Novocure, Pfizer, Roche, and Takeda; payment or honoraria for lectures, presentations, speaker bureau, manuscript writing or educational events from Anheart Therapeutics, AstraZeneca, Bristol-Myers Squibb, Janssen, MSD, Pfizer, Sanofi, and Takeda; payment for expert testimony from AstraZeneca, Bristol-Myers Squibb, Janssen, and Roche; support for attending meetings and/or travel from AstraZeneca, Bristol-Myers Squibb, MSD, Pfizer, Roche, and Takeda; and participated on a data safety monitoring board or advisory board for Pharmamar and Roche. CAV received consulting fees or meeting/travel support from Amgen, AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Lilly, MSD, Novartis, Pfizer, Roche, Sanofi Aventis, and Takeda; and participated in an advisory board for AbbVie, AstraZeneca, Bristol-Myers Squibb, Janssen, Lilly, MSD, Pfizer, Roche, and Sanofi. GJ received meeting/travel support from Sanofi. SH received personal/institutional honoraria from AstraZeneca, Bristol-Myers Squibb, Roche, Sanofi, and Takeda; and meeting/travel support from Novartis and Sanofi. AS received consulting fees from Exafield and Guidepoint; honoraria from Amgen, AstraZeneca, and MSD; meeting/travel support from Amgen and Roche; and is a board member of the SFFPO. EP received personal/institutional honoraria from Amgen, AstraZeneca, and MSD; meeting/travel support from Takeda and Amgen; and participated in an advisory board for Takeda. NG declared research grants/support from AbbVie, Amgen, AstraZeneca, BeiGene, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi-Sankyo, Gilead, Hoffmann-La Roche, Janssen, LEO Pharma, Lilly, Merk Serono, MSD, Novartis, Sanofi, Sivan; consultative services for AbbVie, Amgen, AstraZeneca, BeiGene, Bristol-Myers Squibb, Daiichi-Sankyo, Gilead, Ipsen Hoffmann-La Roche, Janssen, LEO Pharma, Lilly, MSD, Mirati, Novartis, Pfizer, Pierre Fabre, Sanofi, Takeda; participation on a data safety monitoring board for Hoffmann-La Roche; and employment of a family member with AstraZeneca. PDR received meeting/travel support from Boehringer Ingelheim, Daiichi Sankyo, Summit Therapeutics, Sanofi, and Takeda; and participated in an advisory board for Sanofi and Takeda. All other authors have declared no conflicts of interest., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Objectives: Understanding the factors that lead to relapse is a major challenge for the clinical support of smoking cessation. Neurocognitive abilities such as attention, executive functioning and working memory, are possible predictors of relapse and can be easily assessed in everyday clinical practice. In this prospective longitudinal study, we investigated the relationship between pre-smoking cessation neurocognitive performance and relapse at six months in a sample of patients being treated for their tobacco dependence., Methods: 130 tobacco consumers were included in the study. They completed a comprehensive neuropsychological and clinical assessment before smoking cessation. The targeted abilities were intelligence, inhibition, shifting, working memory updating, verbal fluency and decision-making., Results: The rate of tobacco relapse at 6 months was 58%. Logistic regressions were used to assess which variables best explained relapse. None of the neuropsychological tests was a significant predictor of relapse at either 1, 3 or 6 months, either alone, or controlling for other covariates acting as significant predictors of relapse., Conclusions: Common neuropsychological tests, even those specifically targeting executive functioning such as inhibition, are not useful predictors of the success of a smoking cessation program in a clinical setting. Other variables, such as motivation to quit smoking or the presence of comorbid depression or anxiety disorders, appear to be more useful predictors of relapse., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)