Interestingly CpdA in combination with the proteasome inhibitor, Bortezomib (BZ), has been investigated in the context of lymphoma and multiple myeloma cells and shows that BZ enhances CpdA’s dissociated properties and that CpdA on its own prevents down-regulation not only of the GR, but also of FKBP51, a GR chaperone protein upregulated by Dex that is involved in acquired GC resistance67. The gene discussed is NR3C1; the disease is plasma cell myeloma.