To further decipher whether HP1γ protein stability is regulated by acetylation in BR MM cells, we treated WT and BR MM cells with cycloheximide (CHX) for up to 8 h to cease protein synthesis, and found that degradation of HP1γ in BR cells was markedly delayed compared to WT cells (Fig. 2j), which phenotype was similar to what was observed in MM cells stably expressing ectopic HDAC1 (Supplementary Fig. 3a). This evidence concerns the gene HDAC1 and Miyoshi myopathy.