To kill cytosolic invaders, macrophages may utilize antimicrobial effectors such as ubiquicidin (46), interferon-inducible guanylate binding proteins (GBPs) (47), lysozyme (18), or autophagy (48). Unlike the results previously determined with Francisella novicida (47), recent data from our laboratory suggest that GBPs do not contribute to bacteriolysis of L. monocytogenes in the cytosol (49). Although the host factors which restrict cytosolic pathogens are unknown, a recent study found that S. enterica ΔsifA mutants experience oxidative and/or nitrosative stress in the macrophage cytosol (50), although it is unclear whether this stress originates from the host, from the bacterium, or from both. Our findings suggest that, despite increased sensitivity to ROS, cytosolic ROS is unlikely to be responsible for survival of L. monocytogenes MK-deficient mutants (Fig. S6C to E). Finally, in addition to identifying novel targets for therapeutic intervention, L. monocytogenes mutants susceptible to killing in the host cytosol act as tools to identify the host pathways responsible for killing these mutants.