We previously reported that IL-1β/IL-1R1 signaling contributes to cognitive deficits post-CHI and that genetic deletion of IL-1R1 improved cognitive outcomes post-CHI.6 Given that nVNS may reduce IL-1β activation,26–29 it became a strong candidate for therapies treating/preventing secondary sequelae of CHI. The gene discussed is IL1R1; the disease is congenital isolated hyperinsulinism.