To ask whether the inhibitory effect of TA on monocyte adhesion is dependent on KLF2, we used KLF2 siRNA to knockdown KLF2 in ECs and examined its effect on monocyte adhesion. The efficiency of KLF2 siRNA (20 nM) to knockdown KLF2 in endothelial cells was analyzed by qPCR, and the results showed that about 70% KLF2 knockdown was achieved (Fig. 4C). When cells were transfected with control siRNA, TNFα significantly induced monocyte adhesion to HUVECs, and TA treatment significantly attenuated TNFα-induced monocyte adhesion (Fig. 4D,E), which was in consistent with Fig. 4A,B. When cells were transfected with KLF2 siRNA, the inhibitory effects of TA on TNFα-induced monocyte adhesion to endothelial cells was significantly reduced compared that with control siRNA treatment (Fig. 4D,E). Our results suggest that TA represses TNFα-induced monocyte adhesion at least in part via KLF2.