Autonomic neuropathy affects 60% of CKD patients and, along with sustained hyperglycemia-induced protein kinase C (PKC) activation, contributes to micro- and macrovascular damage, redox stress, and diabetic microvascular complications such as nephropathy, altered blood flow, permeability changes, extracellular matrix accumulation, basement membrane thickening, and angiogenesis [17,18,19]. The gene discussed is PRRT2; the disease is chronic kidney disease.