If this is the case, glucagon secretion defects similar to those observed in Fh1βKO mice should also develop in other models of hyperglycemia. We tested this using an inducible mouse model of neonatal diabetes with β cell-specific expression of an activating KATP channel mutation (Kir6.2-V59M) (βV59M) (Brereton et al., 2014). The gene discussed is KCNJ11; the disease is Hyperglycemia.