Initially, the heightened oxidative stress response to hyperglycemia triggers a cascade of effects, culminating in alterations to the signaling pathways, such as the protein kinase C (PKC) pathway, advanced glycation end products (AGEs) pathway, activation of glycolytic polyol pathways, and the overproduction of reactive oxygen species (ROS) [8,9]. This evidence concerns the gene PRRT2 and Hyperglycemia.