Data reported so far showed that (1) the ACE I/D polymorphism directly influences circulating levels of ACE, (2) the II genotype protects against the development of diabetic nephropathy, (3) the DD genotype predicts poor renal response to RAAS inhibitors (the current strategy of RAAS inhibition in patients with the DD genotype may be insufficient to block an activated RAAS), and (4) angiotensin II type 1 receptor blockers (ARBs) can ameliorate the adverse effect of the D allele (no difference between genotypes is observed when patients are treated with an ARB). Here, ACE is linked to diabetic kidney disease.