Other upstream pathways activating PKC and subsequently NOX include those of diabetic nephropathy, where advanced glycation end products (AGEs) or advanced oxidation protein products (AOPPs) increased PKC activity, particularly of PKC-α, with resulting increases in NOX (Williams, 2007; Thallas-Bonke et al., 2008; Wei et al., 2009). The gene discussed is PRRT2; the disease is diabetic kidney disease.