Given that cohoused WT and Mavs−/− or Stinggt/gt mice harbored similar intestinal bacterial populations, it is unlikely that differences in bacterial composition contributed to the protective role of MAVS or STING during GVHD development, unlike what has been proposed for IFN-I–mediated control of Paneth cell function (33). Here, STING1 is linked to graft versus host disease.