Thus, the aim of this study was to examine the renoprotective role of deletion of Nox4 and in particular to examine potential downstream mediators of renal injury that are attenuated upon loss of Nox4 signaling, in particular, with a focus on cytosolic and mitochondrial ROS generation as well as the evaluation of PKC‐α and PKC‐β, which mediate various functional and structural features of DN. This evidence concerns the gene PRKCB and liver dysplastic nodule.