Consistent with what we observed with HSV-1, exogenous IFN-α stimulation still suppressed VSV-GFP infection in both Ctrl and RanBP2-dE3-1 cells, and the efficiency of VSV-GFP infection was significantly lower in RanBP2-dE3-1 cells compared to Ctrl cells after exogenous IFN-α stimulation (Figure 5D–F). Here, RANBP2 is linked to infection.