In contrast, Rec-1 cells appeared to activate NF-κB through the PIR pathway, where despite proteasome inhibition by bortezomib, DNA-binding by largely p50/cRel heterodimers was not inhibited; similar to our observations in the WEHI231 murine B-cell lymphoma cell line which displays a high-level of proteasome inhibitor resistant constitutive NF-κB activity [43-46,56-58]. The gene discussed is REL; the disease is B-cell non-Hodgkin lymphoma.