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). The gene discussed is XPO1; the disease is AL amyloidosis.