Deletion of glucose-regulated protein 78 (GRP78), a key regulator of ER homeostasis, causes AT2 cells to undergo ER stress, apoptosis, senescence, impaired stemness, and TGF-β/Smad signaling activation; moreover, GRP78 is severely deleted in AT2 cells of IPF patients [44]. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.