Furthermore, the loss of p53 function via deletion, mutation or genetic silencing resulted in a complete loss of VMY-induced cytotoxicity in a variety of cancers, including prostate, breast and pancreas, while re-expression of wild type p53 in PC3 cells or treatment of DU145 cells with PRIMA1 restored VMY-induced autophagy and cell death [11, 15]. Here, PRIMA1 is linked to cancer.