Whereas deleting endothelial Ceacam1 did not affect insulin-stimulated insulin receptor phosphorylation in isolated liver endothelial cells, it deactivated the IRS-1/Akt/eNOS pathway to reduce eNOS-mediated NO production, a hallmark of endothelial dysfunction, as was manifested in global Cc1−/− nulls by reduced endothelium-dependent relaxation in aortae [16] and microvasculature [7]. The gene discussed is AKT1; the disease is endothelial dysfunction.