This phenomenon may be due to: i) activated AKT by hyperinsulinemia (48, 49), ii) activated PKA (22, 42) by hyperglucagonemia (50, 51, 52), iii) hyperglycemia (43), and iv) activated AMPKα1/2 increasing the negative AMPKα1/2 phosphorylation at S496/491 to inhibit AMPK activity. This evidence concerns the gene PRKAA1 and hyperinsulinism.