Endoplasmic reticulam is an imprtant organelle in cells. Normal functions of the ER could be impaired and that causes endoplasmic reticulam stress (ERS). ERS activates unfolded protein response (UPR), including immediate stoppage of new protein synthesis, up-regulation of ER chaperones and folding enzymes, and inducement of ER-associated degradation as a self-protective mechanism and induces rescue or adaptive response. If stress is prolonged and functions of the ER are severely impaired, to protect the organism by eliminating the damaged cells, apoptotic signals are generated through several mechanisms including: induction of C/EBP homologous protein CHOP, IRE-1-mediated activation of ASK1/JNK, cleavage and activation of procaspase-12 and Bcl-2-regulated Ca²⁺ release from the ER.