Similar defects in glucagon secretion develop in other diabetic models: transgenic mice that express a human neonatal diabetes mutation (Kir6.2-V59M) specifically in β cells (Brereton et al., 2014) and Goto-Kakizaki (GK) rats, a model of polygenic diabetes (Granhall et al., 2006). The gene discussed is KCNJ11; the disease is diabetes mellitus.