In this regard, the selective overexpression of human ACE2 in the podocytes attenuated the development of nephropathy in mice with streptozotocin-induced type 1 diabetes, and compared with wild-type diabetic mice, these mice experienced less glomerular injury, a delay in developing albuminuria, a blunted decrease in the podocyte markers nephrin and synaptopodin, and protection against podocyte loss (Nadarajah et al., 2012). The gene discussed is ACE2; the disease is kidney disorder.