Activation of the renin-angiotensin system (RAS) has been demonstrated to be involved in both the pathogenesis of CKD and its cardiovascular complications, and blockade of the RAS by angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II (Ang II) type 1 receptor (AT1R)-specific blockers (ARB) has been shown to exert various protective effects on CKD progression and cardiovascular complications, at least partially, through a reduction in urinary protein/albumin excretion [11–14]. The gene discussed is REN; the disease is chronic kidney disease.