The significantly enriched processes included the BP category of cell migration (RAB1A, PTEN, FOXC1, etc.), positive regulation of cell proliferation (GCNT2, HGF, FGFBP1, etc.), extracellular matrix organization (VCAM1, COL9A1, SMOC2, etc.), and negative regulation of I-kappaB kinase/NF-kappaB signaling (RIPK1, TLE1, TNIP3), which were all involved in the pathogenesis of TAO (Figure 3B). The gene discussed is FOXC1; the disease is thromboangiitis obliterans.