In this study, we found that Nox4 deficiency attenuated the expression of proinflammatory cytokines in SMCs and the migration of SMCs in response to flagellin stimulation, indicating that the flagellin-TLR5-Nox4 signaling cascade is an important mediator in the formation of intimal hyperplasia in atherosclerosis (Fig. 7). Here, NOX4 is linked to atherosclerosis.