TP53 and cancer: We speculated that the difference in apoptosis induction may relate to the status and abundance of mutation of p53 [41], while the prosurvival effect of bcl-2 might retreat to the back of the p53, playing a secondary role in response to chemotherapeutic agent because mutant p53 (mutp53) cancers are dependent on their hyper stable mutp53 protein for survival (Figures 4 and 7) [4]; this might endow Kyse 150 cell less sensitive than Kyse 450 cell.