An in vitro study using human coronary endothelial cells from angiographically proven coronary artery disease revealed that A-FABP could enhance the expression of intracellular adhesion molecule-1, vascular adhesion molecule-1, and P-selectin through the ERK/JNK/STAT-1 signaling pathway as well as by suppressing the activation of endothelial nitric oxide [34]. The gene discussed is STAT1; the disease is coronary artery disorder.