The loop diuretic, bumetanide impaired GLP‐1 secretory response by glycine without affecting glucose‐triggered secretion suggesting that the bumetanide‐sensitive Na‐K‐Cl cotransporter maintains high intracellular Cl−concentrations in the GLUTag cells.97 The angiotensin receptor blocker (ARB), olmesartan improved glucose intolerance independent of improvements in muscle and/or adipose insulin signalling, which could be attributed to increasing GLP‐1 concentration and pancreatic GLP‐1 receptor expression thereby improving glucose‐dependent insulin secretion.98 The gene discussed is GCG; the disease is Glucose intolerance.