For example, hyperglycemia could accelerate polyol pathway flux, alter cellular redox state, increase formation of diacylglycerol (DAG) and the subsequent activation of protein kinase C (PKC) isoforms and augmented non-enzymatic formation of advanced glycated end products, which cause the extracellular matrix to change and induce hypertrophy of cardiomyocytes, microangiopathy of heart, fibrosis of interstitial substance, which eventually leading to heart failure[4,5]. Here, PRRT2 is linked to Hyperglycemia.