We further identified that erianin exerted its anti-tumor activities via distinct mechanisms: a) In LNCaP cells, it activated multiple early and late UPRs, indicative of ER stress, which was associated with upregulation of pro-apoptotic Bcl-2 family members, Bim and Bax, and downregulation of anti-apoptotic Bcl-2 and its sibling protein Mcl-1, leading to the execution of apoptosis as reflected by cleavage of caspase-3 and PARP. The gene discussed is MCL1; the disease is neoplasm.