While Romacho et al. reported that DPP-4i improves endothelial function by activation of PAR2 (protease-activated receptor 2) and release of thromboxane-A2 in mice [64], Nomoto et al. provided evidence indicating that DPP-4i does not improve endothelial dysfunction [65], suggesting that more evidence is needed to show beneficial effects of these agents on endothelial function. The gene discussed is F2RL1; the disease is endothelial dysfunction.