Our previous studies showed that AngII mediates the profibrotic effect of hyperoxia on cultured human lung fibroblasts and that ACE-2, which protects against lung fibrosis in animal models by degrading AngII, is downregulated in the lungs of patients with Idiopathic Pulmonary Fibrosis through mechanisms yet to be fully identified. The gene discussed is ACE2; the disease is pulmonary fibrosis.