STING1 and infection: Since type I IFNs could induce the activation of STAT3, which is a key mediator of anti-inflammatory signaling (221), the cGAMPs-STING-type I IFNs axis may be the underlying mechanism, through which biofilms render the host an anti-inflammatory state, thereby resulting in the persistent biofilm-mediated infections in an immunocompetent host (222).