Notably, while m6A clearly governs PD-L1 expression in multiple tumor-intrinsic contexts, direct causal links from CAF m6A machinery to tumor PD-L1 are still sparse; where PD-L1 rises after CAF–tumor crosstalk, the current best-supported mechanisms are AKT signaling and miRNA-bearing exosomes, with m6A often acting upstream on metabolism and stress adaptation that secondarily shapes immunosuppressive tone. This evidence concerns the gene AKT1 and neoplasm.