Smad3/IκBα signalling is the main downstream mediator and responsible for the anti‐inflammatory effects of TGFβ1.11 The enhancement of Smad3 phosphorylation and nuclear expression can increase NF‐κB inhibitor alpha (IκBα) degradation and nuclear factor‐kappa B (NF‐κB) activation, which thus promotes the inflammatory reaction and atherosclerosis.12 Here, SMAD3 is linked to atherosclerosis.