STING1 and infection: This inhibition of IL-1β processing by type I IFN has been shown to limit host defense to M. tuberculosis, Candida albicans, and Group A Streptococcus, and is likely the mechanism by which STING-dependent type I IFN is limiting IL-1β production in response to S. aureus. Understanding how S. aureus triggers immune pathways and the relative contributions of known and/or novel PRR pathways to S. aureus-initiated transcriptional cascades may lead to novel strategies to combat infection.