Prior work in colonic epithelial and colorectal cancer models has established that PAR-2 activation exerts robust anti-apoptotic effects, whereas PAR-2 silencing or pharmacologic inhibition restores caspase-8/-3 activation and enhances susceptibility to cytokine- or chemotherapy-induced apoptosis [43,63,64,65]. The gene discussed is CASP8; the disease is colorectal cancer.