Using AECII specific Sohlh2 CKI mouse model, we confirmed that Sohlh2 overexpression caused mitochondrial damage in AECIIs and spontaneous lung fibrosis, and Sohlh2 in AECIIs also largely enhanced HFD-driven oxidative stress, fibrotic remodeling, inflammation, and cell death. The gene discussed is CHKA; the disease is pulmonary fibrosis.