Ho et al. [102] found that HDAC3 knockdown (KD) in BMSC obviously reduced exosome release from a MM-BMSC co-culture model owing to the downregulation of TSG101, and further down-modified the expression of pro-survival miRNAs (such as miR380, miR382, miR15b, miR9986, and miR5191) in these exosomes, indicating the potential to inhibit MM progression via targeting MM-BMSC paracrine-autocrine signaling crosstalk. Here, HDAC3 is linked to Miyoshi myopathy.