Dear Editor,The expression of myosin heavy chain 10 (MYH10) in atherosclerosis (AS) was positively correlated with the number of vascular smooth muscle cells (VSMCs), which were negatively related to the AS measured by intima-media thickness (IMT). MYH10 might be a potential biomarker for clinical AS, which was the formation of fibrous fatty lesions in the arterial wall. Over time, atherosclerotic plaques become more fibrotic. 1 Advanced atherosclerotic plaques can invade arterial cavities, block blood flow, or form clots, resulting in tissue ischemia. 2 Although some progress has been made in the treatment of AS, drugs and arterial interventional therapy cannot target the pathogenesis and progression of the disease, and there are risks of postoperative thrombosis and restenosis. 3,4 Because of the complexity of its pathogenesis, gene therapy is still in the stage of basic research and is still a serious challenge in modern medicine.VSMCs are one of the main cells that form the tissue structure of the vascular wall and maintain vascular tension. Studies have shown that the origin, phenotypic transformation, apoptosis, and calcification of VSMCs are closely related to AS. 5 Some scholars believe that phenotypic transformation of VSMCs plays an important role in the formation of AS, and inhibition of phenotypic transformation of VSMCs has a protective effect on arteries. 6 Under normal conditions, VSMCs in the arterial middle layer can express smooth muscle cell markers, such as myosin heavy chain 11 (MYH11), MYH9, MYH10, and αsmooth muscle actin (α-SMA), but the ability of VSMCs in the arterial middle layer with AS to express these markers is decreased. 7 MYH10 (Myosin Heavy Chain 10) is a member of the Myosin superfamily. 8 This protein represents a conventional non-muscle myosin. Myosin is an actin-dependent motor protein with a variety of functions, including regulation of cell division, cell movement, and cell polarity. 9This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.