In this study, we demonstrate that the upregulated METTL3 expression in CRC results in aberrant m6A modification, and that methylation of EphA2 and VEGFA by METTL3 via different IGF2BP-dependent mechanisms induces VM formation to promote CRC progression by activating both PI3K/AKT and ERK1/2 signaling (Fig. 7). This evidence concerns the gene AKT1 and colorectal carcinoma.