Furthermore, FAK is highly conserved during evolution and widely expressed in different cells, FAK protein levels are increased in adipocytes of insulin-resistant mice which relate to adipose tissue expansion, leading to obese (Luk et al., 2017), FAK also can be activated by TNF-α in vascular smooth muscle cells which is involved in the process of atherosclerosis restenosis (Yu et al., 2018), suggesting that activation of FAK may increase not only in abnormal vascular endothelial cells and smooth muscle cells, but also in whole aorta of atherosclerotic ApoE−/− mice (Chen et al., 2018). The gene discussed is INS; the disease is atherosclerosis.