Apart from glucose metabolism, several mechanisms have been identified to contribute to myocardial fibrosis, cardiomyocyte injury, and remodeling in DM, such as the activation of the renin–angiotensin–aldosterone system and sympathetic activity, altered myocardial insulin signaling, mitochondrial dysfunction, gene dysregulation of microRNAs and transcription factors, epigenetic modifications, oxidative stress, and endoplasmic reticulum stress [32]. Here, INS is linked to diabetes mellitus.