Our results show that OFs in TAO maintained higher activity of the NF-κB pathway (Fig 4), expression of IGF-1 was dependent on the NF-κB pathway (Fig 5), and that octreotide inhibited phosphorylation of IKKα/β and p65, and degradation of IκB in OFs from TAO patients (Fig 6). The gene discussed is NFKB1; the disease is thromboangiitis obliterans.