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. This evidence concerns the gene AGT and pulmonary fibrosis.