“…Downstream targets of p53 include members of the B-cell lymphoma 2 (Bcl-2) family of proteins involved in regulating intrinsic apoptosis [ 79 ]. Thus, DATS treatment is known to increase apoptosis by regulating expression of pro-apoptotic Bcl-2-like protein 4 (Bax) [ 38 , 41 , 44 , 45 , 46 , 50 , 61 , 66 , 67 , 71 , 72 , 78 , 80 ], Bcl-2 homologous antagonist (Bak) [ 38 , 50 , 70 , 72 ], BH3 interacting domain death agonist (Bid) [ 38 ], Bcl-2-associated death promoter (Bad) [ 57 ], p53 upregulated modulator of apoptosis (PUMA) [ 50 , 80 ], and phorbol-12-myristate-13-acetate-induced protein 1 (NOXA) [ 50 ] as well as anti-apoptotic Bcl-2 [ 37 , 38 , 41 , 44 , 45 , 50 , 57 , 61 , 66 , 67 , 70 , 71 , 76 , 78 , 80 , 81 , 82 ] and B-cell lymphoma-extra large (Bcl-XL) [ 38 , 45 , 50 , 70 , 78 , 82 ]. Moreover, the pro-apoptotic protein Bcl-2-like protein 11 (Bim), which is a downstream target of JNK, displayed increased phosphorylation following DATS incubation thus providing one connection between DATS treatment, ROS generation, and induction of apoptosis […”