Downstream of these, and in MF/SS lesions, signaling mediators such as TRAF proteins and kinases such as TAK1, can trigger NF-κB activation and control malignant T-cell responses and important biological activities, including differentiation toward Th1, Th2, and Th17 cell lineages [71,74]. The gene discussed is NFKB1; the disease is synovial sarcoma.