In 10–37 % of ECs, an activating mutation is reportedly found in codons 12 or 13 of the K-ras proto-oncogene, and also in 6–16 % of atypical hyperplasia, but not in normal endometrium; this implies that CD44 affects early-stage EC oncogenesis—more in well-differentiated cancers of endometrioid morphology [24, 40]. This evidence concerns the gene KRAS and cancer.