Accordingly, in light of combination with the above findings, we hypothesized that CV-A16 infection produces a sequential event, that is, CV-A16 may be recognized by TLR3, RIG-I, and MDA5, which in turn leads to the activation of NF-κB, which further mediates the expression of an array of inflammatory cytokine genes. Here, NFKB1 is linked to infection.