δ- & γ-tocotrienols exerted potent anti-cancer activities as compared to α-tocotrienol.γ-tocotrienol induced mammary tumor cell apoptosis in JNK- & p38-mediated CHOP and DR5-dependent manner.ERS was involved in the upstream mechanism of tocotrienol-induced apoptosis as evidenced by the upregulation of ATF4, CHOP, and Grp78 levels; and Xbp-1 mRNA splicing. ERS inhibitor (salubrinal) protected the cells from γ-tocotrienol-induced MAPK activation and apoptosis. The gene discussed is DDIT3; the disease is breast cancer.