IFNG and infection: Thus, PIM1 operates bidirectionally during infection: in uninfected bystander cells it phosphorylates GBP1 to limit membrane damage, and in infected cells PIM1 performs a dual role—on the one hand, the parasite effector TgIST blocks IFN-γ signaling, rapidly depleting PIM1 and unleashing GBP1 onto the parasitophorous vacuole; on the other hand, it inhibits apoptosis, creating a survival-permissive environment for the parasite.