Mechanistically, METTL3 can recruit the HR repair factors RAD51 and BRCA1 to sites of radiotherapy-induced DNA DSB damage through m6A modification to promote HR repair, thereby increasing radioresistance, while BRD7 overexpression inhibits the recruitment of BRCA1 and RAD51 and, in turn, HR repair activity, in NPC cells by decreasing the protein stability of METTL3; this is the mechanism by which BRD7 promotes radiosensitization in NPC cells. This evidence concerns the gene METTL3 and nasopharyngeal carcinoma.