In vivo studies corroborated these findings, with α-mangostin administration (20 and 40 mg/kg) inhibiting tumor growth in a mouse model of cervical cancer by activating phosphorylated apoptosis signal-regulating kinase-1 (p-ASK1), p-p38, cleaved caspase-3, and cleaved PARP in tumor tissues without affecting body weight. The gene discussed is PARP1; the disease is neoplasm.