Our data, together with the findings from other groups, suggest that DSK interfered with cellular redox homeostasis, manifested as a p38-dependent signature of apoptotic proteome, including induction of Nrf2/HO-1 expression and mitochondria-mediated caspase cleavage (caspase-9 and -3), ultimately resulting in elevated cell death of tongue cancer. The gene discussed is NFE2L2; the disease is tongue cancer.