When cancer cells are stimulated by cytotoxic drugs, ultraviolet rays or other stimulus, endogenous cell apoptosis is activated [43], and the conformation of the anti-apoptotic protein changes, prompting cells to release the mitochondrial interstitial protein cytochrome C (Cytc) [41,44], which activates downstream effector molecules caspase-7, caspase-3 and PARP activation proteins Cleaved caspase-7, Cleaved caspase-9, inhibit DNA repair, and ultimately lead to cell apoptosis [45]. This evidence concerns the gene CASP3 and cancer.