Interestingly, Hes and Nar could reduce the clonogenic potential and the viability of MM cells, even resistant to standard-of-care treatments, like PIs, and such anti-MM effects were antagonized by Drp1 overexpression, again confirming a mitochondrial targeting, Drp1-dependent, activity of the two agents. Here, RRBP1 is linked to Miyoshi myopathy.