Atherosclerosis is a chronic inflammatory disease as well as involves both innate and adaptive immune responses.Lipid-laden "foam cells" is primary component of the earliest atherosclerotic lesions.Act1,known as NF-κB activator 1,lies upstream of IKK and JNK,and mainly mediates classic IL-17/NF-κB signaling pathway.However,whether Act1 involved in the development of atherosclerosis was still unknown.Our data demonstrated that specific Act1 inhibition in macrophages effectively reduces atherosclerotic plaque in vivo and foam cell formation induced by ox-LDL in vitro.Furthermore,Actl inhibition decreases foam cell formation by suppressing ox-LDL uptake via CD-36-dependent pathway in peritoneal macrophages.