Its strong positive correlations with CTLA-4, PD-L1, Tregs, and CD8+ T cells suggest that the CD27 on CD20− B cell subset may drive tumor progression by promoting T cell exhaustion or directly exerting immunosuppressive functions.[26,27] This challenges the traditional view of simplistically categorizing B cells into either antitumor or pro-tumor populations, emphasizing the importance of subpopulation classification based on more refined surface markers such as CD20 deficiency.[28]. This evidence concerns the gene CD27 and neoplasm.