It has been proposed that decreased OXPHOS activity may contribute to T2D development by causing fatty acid accumulation in muscle cells, which in turn may inhibit insulin-stimulated glucose uptake [1], [2], [7], [8], [11], or by indirectly reducing glucose-stimulated insulin secretion from pancreatic ß-cells due to a decrease in ATP production [1]. Here, INS is linked to type 2 diabetes mellitus.