TBK1 and neoplasm: Given IFN‐I responses from the host play a crucial role in all stages of tumorigenesis and progression,[24] and abolishing GRA4 in ME49 enhances host IFN‐I responses by targeting TBK1, we hypothesized whether the value of GRA4 deficient T. gondii in enhancing IFN‐I production could be applied to host tumor immunotherapy.