Considering the rapidity by which translational repressor 4E-BP1 is inactivated (within an hour) and the ability of RSVA2 to negate the effects of MEKi on ISGs (i.e. IRF1), these events might partly explain the absence of positive modulation of IFNL1 gene following RSVA2 infection. This evidence concerns the gene EIF4EBP1 and infection.