Numerous cytokines can induce proinflammatory chemokines, and heightened proinflammatory cytokine and chemokine responses have been reported following viral infection of IL-22−/− mice (Guabiraba et al., 2013), suggesting that alternate proinflammatory/antiviral mechanisms compensate for the absence of the IL-22R signaling in knockout mice, whereas such compensatory mechanisms are absent after IL-22 neutralization in WT mice. This evidence concerns the gene IL22RA1 and viral infectious disease.