In T1D subjects, there is an increased activity of the renin–angiotensin–aldosterone system (RAAS) that causes an increase in cardiac fibrotic remodeling; in a 2008 study by Sing et al., T1D was induced in rats by injection of streptozotocin: after 1 week of hyperglycemia, a significant increase in angiotensin 2 levels was detected in streptozotocin-treated rats, which in turn led to increased cardiomyocyte apoptosis and fibrosis [57]. The gene discussed is AGT; the disease is type 1 diabetes mellitus.