Similarly, previous results have highlighted that therapy based on long-acting GLP-1R/GCGR dual agonist, named DualAG, exerted cumulative effects on food intake in rodents, thus reverting the obesity condition together with an amelioration of glucose tolerance [217]; however, these effects were ablated when both GLP-1R and GCGR were genetically eliminated [217]. The gene discussed is GLP1R; the disease is obesity due to melanocortin 4 receptor deficiency.