In endometrial cancer, a decrease in the m6A mRNA methylation in the mRNA transcripts of the important Akt-mTOR pathway components PHLPP2 (a phosphatase causing Akt dephosphorylation and inactivation) and mTORC2 (which phosphorylates and activates Akt) due to a hotspot R298P mutation in METTL14 and simultaneous downregulation of METTL3 contributed to increased proliferation and tumorigenicity. This evidence concerns the gene METTL3 and endometrial cancer.