Moreover, development of lung fibrosis in response to bleomycin, which is accompanied by UPR activation, nuclear Chop induction, and apoptosis in the AECII of treated mice [26, 56], has been observed by three independent groups to be abolished in homozygous Chop(−/−) ko mice [26, 56, 57]. The gene discussed is DDIT3; the disease is pulmonary fibrosis.