Consistent with CEACAM1′s positive role on insulin uptake via its receptor and targeting to its degradation pathways (reviewed in [1]), mice with liver-specific Ceacam1 deletion display primary reduction in insulin clearance and hyperinsulinemia at about 2 months of age, followed by hepatic insulin resistance (partly caused by downregulation of insulin receptor levels in hepatocytes) and steatohepatitis at 6–7 months of age [106]. The gene discussed is INSR; the disease is Hyperinsulinemia.