PRRT2 and Hyperglycemia: Independent of this mechanism, the attenuation of chronic hyperglycemia reduces damage to a number of cell types through several pathways, such as the augmented formation of advanced glycation end-products (AGEs) and its respective receptor, polyol pathway flux, the overactivity of the hexosamine pathway, activation of protein kinase C (PKC) isoforms and even mitochondrial dysfunction (Wright et al., 2006; Giacco and Brownlee, 2010; Alam et al., 2014), which attenuates progressive damage to major target organs.