Many studies tried to investigate whether these defects could be the result of defective GIP and GLP-1 secretion, but evidence failed to identify a uniform GIP and GLP-1 secretion impairment in T2D (7, 8): this is in line with our findings, confirming similar absolute GIP and GLP-1 secretion in NGT and IGT subjects compared to newly diagnosed T2D patients without diabetes-related complications, thus excluding the possible impact of impaired gastric emptying rates as well as possible chronic kidney disease-related modifications of incretins clearance. The gene discussed is GLP1R; the disease is chronic kidney disease.