Analogously, M nuclear export through XPO1 is an interesting target based on the fact that RSV mutated in the XPO1-recognized NES of M is not viable, presumably due to the critical requirement for M in the cytoplasm later in infection for RSV virion assembly (Ghildyal et al., 2009a); inhibition of XPO1 using the XPO1 specific inhibitor leptomycin B (LMB) added later in infection reduces RSV virus production 20-fold, underlining the utility of targeting M nuclear export as an approach to inhibit RSV (Ghildyal et al., 2009a). The gene discussed is XPO1; the disease is infection.