To demonstrate that the improved glucose tolerance was attributable to GIP, mice were pre-treated with either a monoclonal GIPR antagonistic antibody or an isotype control revealing that antagonising GIPR abolished the effects of GIP-Cre::hM3Dq activation on ip glucose tolerance (Figure 1L,M), concomitantly excluding significant direct driving of hM3Dq in pancreatic alpha or beta cells, as pancreatic Gip expression has been reported by others, but was not observed in our hands [24,27]. The gene discussed is GIPR; the disease is glucose measurement.