Matias-guiu et al. [8] described the development of non-endometrioid endometrial carcinoma through these possible pathways: (i) de novo, through p53 mutations, loss of heterozygosity (LOH) at several loci, and some other still unknown gene alterations; or (ii) through dedifferentiation of a pre-existing endometrioid carcinoma. The gene discussed is TP53; the disease is endometrial endometrioid carcinoma.