Upon infection, viruses employ diverse mechanisms to prevent the efficient expression of cellular proteins, while viral protein expression could evade these inhibitory mechanisms.[21, 22] During flavivirus infection, the global cellular protein synthesis is almost completely repressed by PKR‐induced phosphorylation of eIF2α,[32, 33] the inhibition of rRNA synthesis,[53] or other diverse mechanisms.[34] Contrary to cellular mRNA, viral mRNA is usually translated efficiently thanks to alternative translation initiation strategies. Here, EIF2A is linked to infection.