Since early expression of type I IFNs is a molecular signature of influenza virus infection (Katze et al, 2002; Shinohara et al, 2008), which regulates IL-27 production upon influenza infection as observed in this study, we can conclude that IL-27 signalling occurs downstream of type I IFNs in the suppression of IL-17A production by γδ T cells, thereby promoting secondary pneumococcal infection. The gene discussed is IL17A; the disease is pneumococcal infection.