(23), emphasized that T2D and obese patients with defective insulin signal transduction were characterized by malfunctioning mitochondria and overactivated autophagy/mitophagy accompanied with increased cytosolic lipid droplets and autophagosomes formation, which subsequently contributed to the excessive release of fatty acids and ultimately the exacerbation of insulin resistance, confirming the existence of a more complex crosstalk between metabolic disorders progression and autophagic pathways. This evidence concerns the gene INS and type 2 diabetes mellitus.