Activation of this STING-dependent IFN-β production results in impaired local clearance of S. aureus. Since IL-1β is critical for neutrophil recruitment to S. aureus infection sites [3,54], the loss of early type I IFN in STINGGt/Gt mice likely accounts for the increase in IL-1β and enhanced neutrophil recruitment at the site of infection. Here, STING1 is linked to infection.