“…Instead, Ran:L E binding is leveraged by consequent activation of a potent Nup phosphorylation cascade, the true cause of trafficking inhibition. This inhibition happens in infected cells even before the virus begins to replicate (6,26). The cascade involves Erk1/2 and p38 kinases and is absolutely dependent on Ran:L E interactions and also on the dual phosphorylation of L E itself, an activity that is a prerequisite, and not a consequence, of the Nup modifications (7,10,15,16,27).…”