The functional components of the mammalian ER stress response. An imbalance between load of client proteins imposed on the ER and its capacity to fold them triggers a tripartite stress response. Genes whose products increase the functional capacity of the ER or enhance ER-associated protein degradation are activated. Translation is inhibited, and the flux of client proteins is thereby attenuated. Cell death pathways are activated. The first two components of the response enhance the resistance of cells to ER stress, whereas the last component is presumably adaptive at the organism level.