Biological differences in underlying T2D aetiology using routinely assessed clinical markers of insulin resistance, such as obesity and/or high triglycerides (OHTG), have been shown to predict less glucose-lowering to DPP4i (6), which amplifies glucose-stimulated beta cell insulin secretion through the endogenous incretin pathway. Here, INS is linked to obesity due to melanocortin 4 receptor deficiency.