After anti‐PD‐1 treatment, CD4+ cells promote normalized vessel formation in the context of antiangiogenic therapy with anti‐VEGFR‐2 antibody.[21] Similarly, in prostate cancer, inhibition of the binding between VEGF and neurophilin‐2 diminishes PD‐L1 expression and enhances antitumor immunity.[53] In the current study, we revealed that YTHDF2 promoted immune evasion and angiogenesis by upregulating PD‐L1 and VEGFA expression. This evidence concerns the gene CD4 and prostate carcinoma.