Preclinical data demonstrate that selinexor reactivates multiple TSPs relevant to MM, inhibits nuclear factor-κB activity, reduces c-Myc levels and reactivates glucocorticoid receptor signalling in the presence of dexamethasone, all of which has the downstream effect of suppressing MM cell growth [1–3, 10]. This evidence concerns the gene NR3C1 and Miyoshi myopathy.