The importance of the level of ACE2 expression in kidney disease causality come from studies of ACE2 inhibition, which worsened glomerular injury in a mouse model of type 1 diabetes [9], presumably due to the removal of a degradative pathway for Ang II, and from ACE2 gene knockout mice (KO) with type 1 diabetes, where accelerated kidney injury was ameliorated by AT1R blockade [10]. This evidence concerns the gene AGTR1 and type 1 diabetes mellitus.