It also disrupts essential pro-inflammatory cytokine feedback loops (e.g., TNF-α, IL-1β), mirroring the immunodeficiency phenotypes observed in genetic models of NF-κB deficiency, such as the p50/p52 double-knockout mice (Wakamatsu et al., 2005; Gupta et al., 2010; Ruocco et al., 2005). The gene discussed is IL1B; the disease is hyperinsulinemic hypoglycemia, familial, 4.