Angiotensin-converting enzyme 2 (ACE2), a homolog of ACE not inhibited by ACEi, counteracts AngII effects by hydrolyzing AngII into Angiotensin 1–7 (Ang 1–7), which in turn protects against DKD by increasing tissue triglyceride degradation and decreasing kidney weight, mesangial expansion, proteinuria, and renal fibrosis (4). The gene discussed is AGT; the disease is renal fibrosis.