In theory, different mechanisms could explain why this drug class effect was assessed, such as the immunomodulatory effect [45] (both via direct DPP4 inhibition [45] and via GLP-1 [46]), the potentially shorter time in which T2DM patients spent in hypoglycemia [47], lower insulin need and the possibility of interference with a weak DPP4–virus binding interaction [6]. The gene discussed is INS; the disease is type 2 diabetes mellitus.