Activation of ER stress is a salient feature of several neurodegenerative diseases.57 In light of our finding that HSPB1 can inhibit ER stress-induced apoptosis through increasing proteasomal degradation of BIM, therapies aimed at increasing this activity may be of value in neurodegenerative diseases in which ER stress has a pathophysiological role. The gene discussed is BCL2L11; the disease is neurodegenerative disease.