The precise mechanism of how FAK inhibition could prevent or inhibit atherosclerosis remains unclear although a pathological role of FAK in atherosclerosis has been reported, such as its activation by remnant lipoproteins through RhoA and s1-integrin [7], by angiotensin II through Akt-mTOR-NF-κB signaling pathway [8], and by oxidized LDL through p90 ribosomal S6 kinase family proteins [9]. This evidence concerns the gene RHOA and atherosclerosis.