Furthermore, METTL3 can promote gastric carcinogenesis by activating the METTL3/m6A/miR-1184 axis via an m6A-dependent mechanism, thereby interfering with the miR-1184/TRPM2 signaling pathway (34).Recent findings indicate that the demethylase ALKBH5, which regulates ZKSCAN3 expression via N6-methyladenosine (m6A) modification, activates VEGFA transcription and facilitates MNNG-induced gastric cancer cell migration, invasion, cancer stem cell (CSC) generation, vasculogenic mimicry (VM), and ultimately, gastric cancer progression (13). This evidence concerns the gene METTL3 and cancer.