Other factors known to interact with and modulate p50 homodimer activity include C/EBP (CCAAT enhancer binding protein) which has been shown to displace HDAC1 and HDAC3 bound to p50 homodimers, abrogating anti-apoptotic gene repression and contributing to aberrant p50 activity in acute myeloid leukemia [21]. The gene discussed is NFKB1; the disease is acute myeloid leukemia.