Because CEACAM1 is a shared element between insulin and VEGF-A signaling, the data showed that altered signaling through CEACAM1-dependent pathways disrupts endothelial cells’ response to insulin and VEGF-A, and in this cell-autonomous fashion, drives profound endothelial dysfunction, which in the absence of insulin resistance did not advance to overt atheroma formation. The gene discussed is INS; the disease is endothelial dysfunction.