PRRT2 and Hyperglycemia: Endothelial cells are more susceptible to hyperglycemia-induced cellular damage than other cell types, including fatty acid oxidation, nitric oxide decrease, oxidative stress, inflammatory activation, and impaired barrier function [4].To date, widely accepted hypotheses regarding the contribution of hyperglycemia to diabetic complications include heightened polyol pathway flux, activation of protein kinase C (PKC) isoforms, enhanced creation of advanced glycation end products (AGEs), and augmented hexosamine pathway flux [35].