γ-tocotrienol was more potent than α-tocotrienol.γ-tocotrienol induced mammary tumor cell G1 arrest and apoptosis.Transcriptomic analysis revealed the involvement of ERS response and UPR pathways.γ-tocotrienol upregulated the Grp78, ATF3 and CHOP levels with ERS markers (ATF4, phosphor-PERK, phosphor-IRE1α & eIF2α but not ATF6). The gene discussed is DDIT3; the disease is breast cancer.