This question needs to be addressed because (1) renin, through activating the prorenin/renin receptor, has been suggested to be a pro-fibrotic mediator in lung fibrosis independent of Ang II19; (2) both AT1 and AT2 receptors are thought to play a role in mediating lung fibrosis21, 23; (3) high blood pressure is well known to have pathological effects on the renal, cardiovascular and pulmonary systems. This evidence concerns the gene AGTR1 and pulmonary fibrosis.