Increased RAAS activation is linked to progression of CKD of different aetiologies, especially diabetic nephropathy (DN),11 15–18 and is mediated by hypertensive injury17 and accelerated renal fibrosis.19 The physiological relevance of this pathway in the progression of CKD has focused attention on RAAS components including ACE, ACE2, AGT, angiotensin II receptor type 1 (AGTR1), angiotensin II receptor type 2 (AGTR2) and renin (REN), as candidate genes for various CKD-related phenotypes. The gene discussed is ACE; the disease is liver dysplastic nodule.