Glucagon receptor (GCGR) signaling helps maintain glucose homeostasis by stimulating hepatic glucose production. Interestingly, in rodent models of type-1 diabetes, hyperglycemia is almost completely mitigated by deletion of Gcgr. Rivero-Gutierrez et al. created an inducible Gcgr knockout mouse model to compare acute and chronic loss of the GCGR during insulinopenic diabetes. Their results demonstrate that engagement of compensatory signals, specifically GLP-1 receptor signaling, rather than loss of GCGR activation per se, attenuates the development of hyperglycemia during insulinopenic conditions.