The findings that NMDARs mediate the effect of leptin, and are themselves able to regulate β-cell excitability via channel trafficking regulation when activated, are particularly exciting, especially in light of the report by Marquard et al. that demonstrated the inhibition of NMDARs stimulated insulin secretion and improved glucose tolerance in a small type 2 diabetes human trial [43]. This evidence concerns the gene INS and type 2 diabetes mellitus.