During influenza infection, the induction of type I IFNs has been shown to be closely related to secondary bacterial pneumonia.13, 14 The current study revealed that SHP2 deletion led to a high level of IFN‐α, IFN‐β and the decreased production of chemokines such as KC and MIP‐2 in the BALF, upon secondary S aureus infection (Figure 2A‐D). The gene discussed is IFNA1; the disease is influenza.