Based on our and others’s findings, we proposed that silencing or pharmacological inhibition of endogenous ANO1 upregulates TNF-α expression, and promotes TNF-α signaling cascade through phosphorylation of FADD, activation of caspase family, and activation of JNK and JUN, thus leading to induction of apoptosis in prostate cancer cells. Here, JUN is linked to prostate carcinoma.