The functional damage of vascular endothelial cells caused by the disturbed flow induces chronic TGF‐β1 accumulation in the vascular wall, and the accumulated TGF‐β1 suppresses the expression of syndecan‐4 by activation of Smad2/3, which contributes to the progression of atherosclerosis [Tull et al., 2006; Nesbitt et al., 2009; Popovic et al., 2009]. This evidence concerns the gene SMAD2 and atherosclerosis.