The improvements in patient glycaemic responses elicited by GLP-1 agonists, or dipeptidyl peptidase inhibitors that retard GLP-1 degradation, within the circulation, or AMPK activators, e.g. metformin or other biguanides40,64,98 and reversal of the pathological effects of NAFLD and NASH by GLP-1 agonists85,99 tend to corroborate the view that GLP-1 deficiency is a cause of metabolic disease. The gene discussed is GLP1R; the disease is metabolic dysfunction-associated steatotic liver disease.