Importantly, our data indicate that the increased collagen types I and III, fibronectin, and OPN levels in kidney from hypertensive rats were reduced after ACE inhibition, indicating that the RAS signaling is an important factor in the development of hypertension and fibrosis and also supporting the early notion from Guan et al. [26] that high levels of Ang II in the unclipped kidney result from enhanced ACE activity. The gene discussed is SPP1; the disease is hypertensive disorder.