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We studied the taxonomy of Pluteus podospileus and similar species using morphological and molecular (nrITS, TEF1-α ) data, including a detailed study of the type collections of P. inflatus var. alneus , Pluteus minutissimus f. major, and P. granulatus var. tenellus . Within the P. podospileus complex, we phylogenetically confirmed six species in Europe, five in Asia, and eight in North America. Based on our results, we recognize P. seticeps as a separate species occurring in North America, while P. podospileus is limited to Eurasia. We describe six new species and a new variety: P. absconditus , P. fuscodiscus , P. gausapatus , P. inexpectatus , P. millsii, and P. notabilis and its variety, P. notabilis var. insignis . We elevate Pluteus seticeps var. cystidiosus to species rank as Pluteus cystidiosus . Based on the holotype of P. inflatus var. alneus , collections of P. inflatus identified by Velenovský, and several modern collections, we resurrect the name P. inflatus . Based on molecular analyses of syntypes of Pluteus minutissimus f. major and a holotype of Pluteus granulatus var. tenellus , we synonymize them under P. inflatus . We also increase our knowledge about the morphology and distribution of P. cutefractus ., Competing Interests: The authors declare no conflict of interest. The funders had no role in the design of the study, in the collection, analysis, or interpretation of data, in the writing of the manuscript, or in the decision to publish the results.

PIM serine/threonine kinases are overexpressed, translocated, or amplified in multiple B-cell lymphoma types. We have explored the frequency and relevance of PIM expression in different B-cell lymphoma types and investigated whether PIM inhibition could be a rational therapeutic approach. Increased expression of PIM2 was detected in subsets of mantle cell lymphoma, diffuse large B-cell lymphoma (DLBLC), follicular lymphoma, marginal zone lymphoma-mucosa-associated lymphoid tissue type, chronic lymphocytic leukemia, and nodal marginal zone lymphoma cases. Increased PIM2 protein expression was associated with an aggressive clinical course in activated B-like-DLBCL patients. Pharmacologic and genetic inhibition of PIM2 revealed p4E-BP1(Thr37/46) and p4E-BP1(Ser65) as molecular biomarkers characteristic of PIM2 activity and indicated the involvement of PIM2 kinase in regulating mammalian target of rapamycin complex 1. The simultaneous genetic inhibition of all 3 PIM kinases induced changes in apoptosis and cell cycle. In conclusion, we show that PIM2 kinase inhibition is a rational approach in DLBCL treatment, identify appropriate biomarkers for pharmacodynamic studies, and provide a new marker for patient stratification.