In the context of epigenetic alterations, aberrant deacetylation of miR-29a/b-1 promoter by histone deacetylases (HDACs), such as HDAC1, HDAC3 [21] and HDAC4 [19] represents a well-documented mechanism by which tumor cells silence miR-29b; consistently, pan HDAC-inhibitors have been found to upregulate miR-29b expression in MM [19], AML [21] and CLL [22]. This evidence concerns the gene HDAC4 and Miyoshi myopathy.