Such a mechanism has been suggested by a recent study showing proteasome inhibition caused H3K27 deacetylation of a SE in control of transcription of the c-MYC proto-oncogene, which resulted in decreased growth of multiple myeloma cells, a blood cancer where proteasome inhibitors are primarily used as therapy (82). This evidence concerns the gene MYC and hematopoietic and lymphoid system neoplasm.