Duca et al. suggested that high-energy/high-fat feeding combined with an obesity-prone phenotype led to reduced endogenous GLP-1 and GLPR activation [7], suggesting that a high circulation TG level may decrease endogenous GLP-1R activation, therefore affecting the treatment efficacy of the DPP-4 inhibitor. The gene discussed is GLP1R; the disease is obesity due to melanocortin 4 receptor deficiency.