An apoptosis event was caused through the treatment of the androgen-refractory human prostate cancer cell lines PC-3 and DU145 and also, it led to a decrease in cell feasibility triggered by a decline in Bcl-2 and Bcl-xL and an enhancement in the active form of the Bax protein, attended by dose-dependent prevention of XIAP, c-IAP1, c-IAP2, and survivin proteins (Shukla et al., 2014b). This evidence concerns the gene BAX and prostate carcinoma.