We nonetheless reasoned that it might be possible to transform epithelial cells and potentially create an ex vivo engineered endometrial carcinoma model by infecting pEECs with an ecotropic MuLE virus expressing shCdkn2a plus HrasG12V, taking advantage of the fact that largely mutually exclusive genetic alterations in KRAS, HRAS, NRAS, BRAF and NF1 occur in about 32% of human endometrial carcinomas (www.cbioportal.org) and loss of function of Cdkn2a in mouse cells allows escape from RAS-induced senescence and transformation [31,32]. This evidence concerns the gene NRAS and endometrial carcinoma.