They also demonstrated that mice with a lung epithelial cell-specific deletion of PTEN-induced putative kinase 1 (PINK1)—a molecule that plays an important role in the maintenance of mitochondrial morphology and function—exhibited dysfunctional mitochondria in type II AECs, vulnerability to apoptosis, and the development of lung fibrosis. Here, PINK1 is linked to pulmonary fibrosis.