A mechanism-based study (NCT02336815) evinced an improved response in multi-refractory multiple myeloma by providing dexamethasone and selinexor [56], an inhibitor of exportin-1 (CRM1) which traps active tumor suppressor proteins in the nucleus and prevents NFκB activation and the translation of oncoprotein mRNAs. This evidence concerns the gene XPO1 and AL amyloidosis.