The resistance to STZ-induced diabetes is therefore likely due to chronic compensatory mechanisms in GCGR−/− mice, mediated by elevation of GLP-1, which increases glucose-stimulated insulin secretion, and FGF-21, which promotes beta cell regeneration and increases peripheral glucose uptake (Omar et al. 2013, Cui et al. 2023). The gene discussed is GCG; the disease is diabetes mellitus.