For this reason, as indicated above, the improvement in T2DM in ZDF rats may have been due to the pathway previously described, which facilitated the increase in muscle glucose uptake by activation of Akt kinase phosphorylation, and the decrease in insulin resistance, as the enhancement in muscle Zn inhibited the negative regulator of the insulin receptor substrate, PTP1B, in accordance with what was established by other authors [14,15]. The gene discussed is PTPN1; the disease is type 2 diabetes mellitus.