First, CAFs can raise m6A activity inside tumor cells without necessarily transferring RNA: in non-small cell lung cancer (NSCLC), CAF-conditioned cues (notably VEGFA) induce tumor-intrinsic METTL3, elevating m6A on RAC3 and driving AKT/NF-κB signaling, invasion, and in vivo growth. The gene discussed is AKT1; the disease is neoplasm.