An alternative mechanism for PPARγ-mediated STAT3 repression has also beensuggested, in which PPARγ agonist treatment of multiple myeloma cells inducesthe corepressor protein SMRT to dissociate from PPARγ; SMRT could then complexwith and inhibit the transcriptional activities of STAT3. This evidence concerns the gene NCOR2 and plasma cell myeloma.