The HDAC4-MEF2C axis has been established in cancer and cartilage,11,42 and a recent study also suggested a role for HDAC5 in attenuating MEF2C transcriptional activity at the sclerostin gene in osteocytes.43 Thus, although, in accord with a positive transcriptional function, deletion of MEF2C in osteoblasts/osteocytes results in diminished SOST expression,15 interaction of DNA-bound MEF2C with HDACs can restrain the positive effects of MEF2C on transcription. This evidence concerns the gene SOST and cancer.