Association of ER stress pathway and autophagy in Proteasome inhibitor mediated cell cycle arrest. Proteasome inhibitor treatment arrests the normal functioning of the proteasome and increases the load of ubiquitinated and misfolded proteins in cancer cells. This accumulation generates unfolded protein response (UPR) and consequently ER stress. ER stress generation enforces cells to be arrested in cell cycle phases and induce autophagy in order to compensate and reduce the non-functional protein load. At this stage autophagy can resolve the normal cell state by digesting the non-functional proteins and promote cancer cell survival or can trigger apoptosis leading to cancer cell death. Autophagy inhibitors 3-MA and Bafilomycin A can modulate the effect of autophagy induced cell cycle arrest or apoptosis in association with PIs.