Additionally, to determinate the host compartment in which IFN-β was necessary, bone marrow transplants from Ifnar1 KO mice to a WT host revealed a requirement for the hematopoietic cells, more specifically the CD11c+ and CD11c- myeloid populations, that in a context lacking IFN-β lost their cross-priming capacity within the tumor microenvironment [294]. This evidence concerns the gene ITGAX and neoplasm.