CGAS and type 2 diabetes mellitus: Considering the accumulating ER stress and oxidative stress in islet β-cells during T2D pathogenesis as discussed above, one could also reason that another trigger of the cGAS–STING pathway in β-cells could be attributed to stress-induced mtDNA release, which thereby contributes to the formation of a proinflammatory microenvironment in the islet and to the loss of GSIS function in β-cells.