While it is established that cross-presenting cDC1 driven by the transcription factor Batf3 are critical for priming CD8+-specific responses (Hildner et al., 2008; Spranger et al., 2015), recent work by us and others have also implicated additional cDC subsets (Duong et al., 2022) or compensatory development of Batf3-independent cDC1 (Tussiwand et al., 2012) in mediating anti-tumor immunity. This evidence concerns the gene BATF3 and neoplasm.