By analyzing the relationship of mutations in m6A regulatory genes with POLE, PTEN, PIK3CA, KRAS, PIK3R1, TP53, FBXW7, and PPP2R1A mutations, we observed that changes in the former were significantly related to alterations in POLE, PTEN, KRAS, TP53, and PPP2R1A. Moreover, EC has heterogenous tumor morphology, clinical parameters, and genetic makeup [28]. This evidence concerns the gene KRAS and neoplasm.