Further studies have demonstrated that WTAP knockdown in AML prolongs the half-life of MYC mRNA by decreasing the level of m6A methylation, and thereby upregulates MYC expression to activate the phosphatidylinositol 3-kinase (PI3K)/protein serine-threonine kinase (AKT) signaling pathway [90]. This evidence concerns the gene MYC and acute myeloid leukemia.