Considering the central role of hyperinsulinemia and hyperglycemia in the development of selective hepatic insulin resistance and in the activation of AKT, ERK1/2, and PYK2 in hepatocytes (Brown & Goldstein, 2008; Fernandez‐Novell et al., 2014), it is conceivable that both factors contributed to the greater stimulation of the kinases in response to β‐AR stimulation. The gene discussed is AKT1; the disease is hyperinsulinism.