Considering that DPP-4 inhibitors increase endogenous GLP-1 to physiological levels (10–25 pmol/L), whereas GLP-1RA reaches higher pharmacological levels (60–90 pmol/L), the difference in elevated GLP-1 concentrations might contribute to the differing efficacies in patients with NAFLD/NASH, though whether tissue distributions are similar for all GLP-1R and what level of GLP-1 exposure produces each effect, are not well known [43]. The gene discussed is DPP4; the disease is metabolic dysfunction-associated steatohepatitis.