A similar association has been detected in endometrial tumors where DNA methylation is related to inhibition of p53-mediated repression of survivin.20 Nevertheless, we found that survivin promoter hypermethylation in obese-derived hASCs was accompanied by a significant decrease in the levels of its mRNA (Figure 3b), indicating that additional regulatory mechanisms should exist to explain the high levels of survivin protein in hASCs from obese subjects. The gene discussed is TP53; the disease is endometrium neoplasm.