Induction of diabetes in wild-type mice has revealed increased levels of angiotensin coverting enzyme 2 (ACE2), which is involved in regulation of the renin–angiotensin–aldosterone system. Diabetes in these animals led to increases in tubular pressure, hyperfiltration and renal hypertrophy. ACE2-knockout mice and those given ACE2 inhibitors resisted this phenotype, and did not have increased creatinine clearance despite a high-protein diet—implicating ACE2 in diabetic nephropathy.