We conclude that the effect of paraoxon treatment on the development of hyperglycemia in the MLD-STZ model is due to a combination of factors: (a) stimulation of insulin production by β-cells and (b) protection against STZ-induced apoptosis, both through the mAChRs, and (c) differentiation of Th1 (T helper 1) cells and mitigation against the development of pathogenic Th17 (T helper 17) cells (36). Here, INS is linked to Hyperglycemia.