In endometrial cancer, the writer METTL3 enhances immunosurveillance by stabilizing the MHC-I transactivator NLRC5, thereby sustaining antigen-presentation gene expression; mechanistically, METTL3-installed m6A prevents YTHDF2-mediated decay of NLRC5 mRNA, and METTL3 overexpression increases intratumoral CD8+ T-cell infiltration and tumor control. This evidence concerns the gene NLRC5 and endometrial cancer.