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Simple Summary: Addressing RB1-deficient cancers poses substantial challenges. Dysfunctional or deleted RB1 can enhance the proliferation and spread of different cancer types. Scientists strive to grasp the intricate role of RB1 in regulating various biological processes and molecular pathways to devise innovative therapeutic strategies tailored to RB1-deficient cancers. Recent advancements have revealed encouraging tactics for combating these malignancies, heralding a path toward more precise and efficacious treatments. This review underscores the pivotal role of RB1 in cancer research and highlights its potential as a focal point for personalized therapies. The retinoblastoma (RB) transcriptional corepressor 1 (RB1) is a critical tumor suppressor gene, governing diverse cellular processes implicated in cancer biology. Dysregulation or deletion in RB1 contributes to the development and progression of various cancers, making it a prime target for therapeutic intervention. RB1′s canonical function in cell cycle control and DNA repair mechanisms underscores its significance in restraining aberrant cell growth and maintaining genomic stability. Understanding the complex interplay between RB1 and cellular pathways is beneficial to fully elucidate its tumor-suppressive role across different cancer types and for therapeutic development. As a result, investigating vulnerabilities arising from RB1 deletion-associated mechanisms offers promising avenues for targeted therapy. Recently, several findings highlighted multiple methods as a promising strategy for combating tumor growth driven by RB1 loss, offering potential clinical benefits in various cancer types. This review summarizes the multifaceted role of RB1 in cancer biology and its implications for targeted therapy. [ABSTRACT FROM AUTHOR]

Phenotypic variation can arise from differences in the protein coding sequence and in the regulatory elements. However, little is known about the contribution of regulatory difference to the expression divergence, especially the cis and trans regulatory variation to the expression divergence in intraspecific populations. In this study, we used two different yeast strains, BY4743 and RM11‐1a/α, to study the regulatory variation to the expression divergence between BY and RM under oxidative stress condition. Our results indicated that the expression divergence of BY and RM is mainly due to trans regulatory variations under both normal and oxidative stress conditions. However, cis regulatory variation seems to play a very important role in oxidative stress response in yeast because 36% of genes showed an increase in cis regulatory variation effect compared with 13% of genes that showed an increase in trans regulatory variation effect after oxidative stress. Our data also indicated that genes located on the longer arm of the chromosomes are more susceptible to cis variation effect under oxidative stress than genes on the shorter arm of the chromosomes. [ABSTRACT FROM AUTHOR]