DOT1L and premature aging syndrome: ZMPSTE24 is a prelamin‐processing zinc metalloproteinase and deficiency of this enzyme in humans results in premature aging syndrome.29 Previous studies have shown that in Zmpste24‐deleted mice, alterations in histone modification affects chromatin organization,30 and in particular, depletion of H3K9 methylation in these mice can rescue bone mineral density (BMD) loss.31 Based on these studies, we evaluated the effects of DOT1L inhibitor EPZ‐5676 in Zmpste24‐deleted mouse forelimbs using μCT.