CIAO2A and infection: We then used rotenone/antimycin A (Rot/AA), which is the mitochondrial electron transport chain complex I/III inhibitor and can promote reactive oxygen species (ROS) production, to treat the cells right before RH infection [23, 24], and the treatment reduced T. gondii load in WT BMDMs but not in Fam96a-deficient BMDMs (Fig 4D), suggesting that Fam96a may regulate the mitochondrial oxidative phosphorylation or related events that involved in control of T. gondii.