The enriched pathways JAK/STAT, IL-6, and interferon signaling are upregulated in CD14 + monocytes isolated from BD patients (59), whereas toll-like receptors 2, 4, and 5 are highly expressed in monocytes, causing a cascade of activation of nuclear factor-κB and production of TNF-α, unveiling a proinflammatory mechanism of BD (60). The gene discussed is SOAT1; the disease is Behcet disease.