Maru et al. investigated the transformation potential of the combination of Kirsten rat sarcoma virus (Kras) activation and Phosphatase and tensin homolog (Pten) inactivation in murine endometrial organoids in the subcutis of immunodeficient mice, and reported that Cyclin-Dependent Kinase Inhibitor 2A (CDKN2A) knockdown or transformation-related protein 53 (Trp53) deletion led to the induction of sarcomatous differentiation and, consequently, to the development of uterine carcinosarcoma [30]. The gene discussed is TP53; the disease is uterine carcinosarcoma.