Such consequences resulted from the reduced infiltration and impaired effector functions of METTL3-deficient NK cells in a tumor niche. Further results demonstrated that METTL3-mediated m6A methylation guaranteed sufficient engagement of AKT-mTOR and MAPK-ERK signaling pathways in response to IL-15 stimulation, presumably through promoting SHP-2 expression. The gene discussed is AKT1; the disease is neoplasm.