The systematic experiments in the present study revealed that (1) DT significantly promoted cell death in the three HNSCCs cell lines; (2) DT induced the cleavage of caspase-3 and caspase-8, and consequently initiated apoptosis in the three HNSCCs cell lines; (3) p38 signaling partially regulated DT-induced apoptosis in Detroit 562 cells; and (4) DT effectively reduced the tumor size in Detroit 562-xenografted mice and did not elicit markedly liver inflammation. The gene discussed is CASP8; the disease is neoplasm.