In addition to the above mechanisms, other studies have shown that the pan-HDAC inhibitor panobinostat or HDAC6 inhibitor ricolinostat can block the function of HSP90, leading to the degradation of PPP3CA (the catalytic subunit of calcineurin, a client protein of Hsp90) and further inactivation of NF-κB signaling, thereby inhibiting the survival ability of MM cells (Imai et al., 2016; Imai et al., 2019). This evidence concerns the gene HDAC9 and Miyoshi myopathy.