In conclusion, we showed that FABP4 can not only cause atherogenesis through the activation of the adhesion molecules, including integrin β2, α4, and PSGL-1 in MNCs and ICAM-1, VCAM-1, and P-selectin in HCAECs, but can also lead to endothelial dysfunction through the activation of the STAT-1 signaling pathways, which in turn may impair the expression/phosphorylation of pro-angiogenic molecules, such as eNOS and SDF-1. This evidence concerns the gene SELP and endothelial dysfunction.