A possible mechanism for synergybetween HDAC and Hsp90 inhibitors involves effects on the survival pathway NF-κB. NF-κB is a transcription factor constitutivelyactivated in many cancer models [31], wherein it confers resistance toapoptosis and promotes cell survival [32], angiogenesis, and invasion [33].Expression profiling studies by us and others have shown that RIPK4, an activator of NF-κB [34], is highly expressed within synovialsarcoma primary tumor samples [35]. The gene discussed is NFKB1; the disease is neoplasm.