TOR1A and liver dysplastic nodule: Through the analysis of two Ins2Akita diabetic mouse models showing different susceptibility to the development and progression of DN, DN-resistant C57BL/6-Ins2Akita (C57BL/6-Akita) and DN-prone KK/Ta-Ins2Akita (KK/Ta-Akita), we have demonstrated that cytoplasmic copper/zinc-SOD (SOD1) is down-regulated in the kidneys of KK/Ta-Akita mice that exhibit progressive DN, but not DN-resistant C57BL/6-Akita mice [11], and that genetic SOD1 deficiency accelerates diabetic glomerular injury in the DN-resistant C57BL/6-Akita mice [12].