Through this m6A‐independent function cooperated with the m6A modification of BCL2 mRNA, ALKBH5 promoted ovarian cancer progression.[23] In this study, we found that ALKBH5 initiated a cluster of prometastatic genes in m6A‐dependent (DEPDC1 and NTSR1) and m6A‐independent (FN1, EGFR, CDH2, ITGA6 and ITGB4) manners. This evidence concerns the gene DEPDC1 and ovarian carcinoma.