α-Mangostin inhibited tumor growth in cervical cancer mouse xenograft models by increasing p-ASK1, p-p38, cleaved-PARP, and cleaved-caspase-3 and inhibiting cell viability. This led to loss of mitochondrial membrane potential (MMP), release of cytochrome C, increase in Bax, decrease in Bcl-2, and activation of the caspase. The gene discussed is BCL2; the disease is cervical carcinoma.