Triptolide has been shown to exhibit antitumor effects in ovarian cancer (SK-OV-3 and SK-OV-3/DDP) cells by inducing autophagy through ROS generation and JAK2/STAT3 pathway inhibition, enhancing chemotherapy sensitivity and inhibiting tumor growth, as well as by inducing apoptosis and reducing the protein expression of MMP-2, Sorcin, and VEGF, thereby disrupting the Mcl-1/Beclin1 interaction and highlighting its multifaceted therapeutic potential [991, 992]. The gene discussed is MCL1; the disease is ovarian carcinoma.