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IFN-\u03b3 exposure improved macrophage survival through the activity of the kinase PIM1. PIM1 phosphorylated GBP1, leading to its sequestration by 14-3-3\u03c3, which thereby prevented GBP1 membrane association. During\n            <jats:italic>Toxoplasma gondii<\/jats:italic>\n            infection, the virulence protein TgIST interfered with IFN-\u03b3 signaling and depleted PIM1, thereby increasing GBP1 activity. Although infected cells can restrain pathogens in a GBP1-dependent manner, this mechanism can protect uninfected bystander cells. 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