These results suggest that dioscin has potential as a targeted drug to promote SHP1 phosphorylation and promote caspase-3 and Bad-related apoptosis by inhibiting the downstream Erk1/2 and P38 signaling pathways (Gajewski and Thompson, 1996; Porter and Janicke, 1999); thus, presenting antitumor effects on PCa. The gene discussed is BAD; the disease is posterior cortical atrophy.