Previous work demonstrated a significant reduction in the density and activity of renal cortical tubular ACE in diabetic compared to control mice [35], whereas increased chymase expression has been observed in humans with diabetic nephropathy [20]; 2) Inability of ACEis to reach the intracellular compartment and suppress the intracrine actions of Ang II initiated from an intracellular location [12]. Here, ACE is linked to diabetic kidney disease.