Indeed, unlike METTL3WT and METTL3K177R reconstitution, which exerted complete rescue effects on defective migration/invasion due to METTL3 loss, METTL3K177Q failed to restore these phenotypes (Supplementary Fig. 4m, n), demonstrating this acetylation-mimetic mutation blocked the nuclear function of METTL3, leading to compromised invasiveness of breast cancer cells. The gene discussed is METTL3; the disease is breast carcinoma.