JCAD (junctional cadherin 5 associated) is an endothelial junction protein that plays critical roles in vascular biology and disease pathogenesis. The protein localizes to endothelial cell-cell junctions and promotes pathological angiogenesis, with JCAD deficiency impairing tumor neovascularization and vascular maturation 1. JCAD functions through multiple signaling pathways, particularly the Hippo-YAP pathway, where it competes with LATS2 for WWC1 interaction, leading to YAP activation and enhanced cell cycle gene expression 2. The protein also modulates PI3K/Akt signaling through direct interaction with Akt, regulating coagulation and fibrinolysis processes 3. JCAD has significant disease relevance, as genetic variants at the JCAD locus associate with coronary artery disease and myocardial infarction risk 4. JCAD deficiency protects against atherosclerosis by improving endothelial function and reducing pro-atherogenic gene expression 4. In thrombosis, JCAD promotes arterial clot formation by enhancing tissue factor expression and reducing fibrinolysis 3. JCAD also contributes to hepatic stellate cell activation and liver fibrosis 5, while playing roles in liver regeneration and cell cycle progression 2. Clinically, elevated plasma JCAD levels correlate with acute coronary syndromes, suggesting potential as a therapeutic target for cardiovascular diseases 3.