VDAC is known to play important roles in the control of ER-to-mitochondria Ca2+ transfer (73) and ATP flux (74) both in β cells and in neurons, with T2D defects associated with VDAC1 mistargeting, which causes loss of ATP flux, mitochondrial Ca2+ dysregulation, and impaired insulin secretion (75). Here, VDAC1 is linked to type 2 diabetes mellitus.