According to this model, normal endometrial cells would transform into endometrioid endometrial carcinoma through 5 different molecular changes, including, mutations of PTEN, PIK3CA, KRAS, and CTNNB1 (β-catenin) genes and microsatellite instability (MSI) while non-endometrioid endometrial carcinoma is frequently related to alterations of p53 and chromosomal instability [7, 8, 15, 16]. The gene discussed is KRAS; the disease is endometrial endometrioid carcinoma.