However, the NF-κB and Smad signaling pathways may be independent of TAAD formation, as evidenced by the parallel phosphorylation levels of IKKβ, NF-κB-p65, Smad1/5, Smad2, and Smad3 between CAD and TAAD patients (Fig. 5d). The gene discussed is SMAD1; the disease is coronary artery disorder.