Both, autophagy-promoting as well as -inhibiting activities of p53, engage the mTOR signaling pathway which in response to genotoxic or metabolic stress cross-talks with p53 in a coordinated fashion [38] Due to our recent finding of a nonsense mutation in p53 that entirely abolishes its expression in uterine sarcoma cells, we concluded that p53 could be the missing link leading to either SAHA-induced autophagy in the absence of the p53 protein or preferential SAHA-stimulated apoptosis when a functional wildtype molecule is present in the cell. The gene discussed is MTOR; the disease is uterine corpus sarcoma.