However, these studies did not determine whether the lack of mAIM-dependent tumor control in Batf3−/− mice was due to a lack of antitumor CTL priming at the time of tumor engraftment, before immunotherapy, or to a failure of mAIM at inducing the reactivation of previously primed but exhausted antitumor CTLs, at the time when the immunotherapy was administered. This evidence concerns the gene BATF3 and neoplasm.