These results suggest that Atiprimod suppresses STAT3 phosphorylation directly, and that this effect is not dependent on the inhibition of NF-κB. Nevertheless, the ability of Atiprimod to inhibit NF-κB, a proven target in myeloma treatment, suggests that Atiprimod might also inhibit myeloma cells through that mechanism, provided that higher concentrations of this drug are used. This evidence concerns the gene NFKB1 and plasma cell myeloma.