These results also showed that METTL3 interacted with γ-H2AX and localized to sites of IR-induced DNA damage in NPC cells and that overexpression of BRD7 inhibited the accumulation of METTL3 at sites of IR-induced DNA damage (Figure 4A-B), suggesting that the BRD7/METTL3 axis is required for the repair of IR-induced DSBs. This evidence concerns the gene H2AX and nasopharyngeal carcinoma.