The above experimental findings on the effect of Nutlin on wild-type p53 tumors can be roughly summarized as follows: the binding of Nutlin to Mdm2, by inactivating the main antagonist of p53, leads to increasing the p53 level, which negatively influences the tumor growth, in part because of the onset of cell arrest and apoptosis, in part – for stem cell-based tumors – by establishing in cancer stem cells a more physiological pathway of asymmetric cell division. The gene discussed is TP53; the disease is cancer.