First, directionality diverges for METTL3 across cancer types: in CRC models it amplifies chemokines linked to myeloid influx, while in endometrial tumors it preserves NLRC5-driven MHC-I and correlates with higher CD8+ content—differences likely rooted in target selection and reader competition that are not yet mapped at base-resolution in primary human specimens. This evidence concerns the gene METTL3 and cancer.