Suzuki et al. [60] reported that different organoselenium compounds, i.e., MSC, SeMet, and Se caused differential apoptotic response of human cancer cells, in that Se-induced apoptosis in carcinoma cells is basically a caspase-dependent process involving the activation of both the intrinsic apoptotic pathway and ER stress pathway, while SeMet-induced apoptosis appears to be mediated via p53 activation. The gene discussed is TP53; the disease is carcinoma.