This speculation is mainly based on the observations that angiotensinogen and Ang II levels are increased in patients with lung fibrosis and relevant animal models20, 21, on in vitro studies showing that Ang II or renin is able to induce lung fibroblast proliferation and ECM production, and on intervention studies showing that blockade of the RAS can ameliorate lung fibrosis. The gene discussed is AGT; the disease is pulmonary fibrosis.