Preclinical data suggested that combining selinexor with proteasome inhibitors and dexamethasone had a mechanistic rationale (Turner et al., 2016a; Kashyap et al., 2016), as XPO1 is overexpressed in multiple myeloma and correlates with increased bone disease and shorter survival (Tai et al., 2014; Tiedemann et al., 2012), a genome-wide RNA interference screen identified XPO1 as an essential gene required for myeloma cell survival and proliferation (Schmidt et al., 2013). This evidence concerns the gene XPO1 and plasma cell myeloma.