Findings in bleomycin-treated mice and AECII of IPF lungs have shown that a disruption in the crosstalk between ER and mitochondria occurs, probably involving mitochondrial homeostasis-control mechanisms, ER stress induced by PINK1, and integrated stress response transcription factors 3 and 4 (ATF3 and ATF4) (130, 133). The gene discussed is PINK1; the disease is idiopathic pulmonary fibrosis.