Postulated mechanisms explaining this synergy between Hsp90 inhibitors and fludarabine include downregulation of antiapoptotic proteins as a consequence of AKT/NFκB inhibition [45] or downregulation of DNA repair enzymes and checkpoint regulators that limit the capacity of CLL cells to repair fludarabine-induced DNA damage [61]. The gene discussed is NFKB1; the disease is B-cell chronic lymphocytic leukemia.