Autophagy, other inflammasomes, such as NLRP3 and Caspase-11, and pro-inflammatory cytokines, such as TNF and IFNγ, have all been implicated in S.Tm infection.27,29,31,62–69 However, in littermate-controlled infections, we found that these factors/pathways were dispensable for restriction of epithelial S.Tm loads in the presence of functional NAIP/NLRC4 (i.e., in a WT mouse background) at 18 h p.i. (Fig S7B–E, and refs. 39,68). The gene discussed is IFNG; the disease is infection.