In general, those KRAS or PIK3CA mutations activate RAS/MAPK or PI3K/AKT pathways and are associated with tumor growth, proliferation, and metastasis [23], but the triggering molecular mechanisms through which KRAS- or PIK3CA-mutated normal endometrium becomes endometriosis and carcinogenesis of EC and CCC from endometriosis is still unclear. This evidence concerns the gene KRAS and neoplasm.