This cascade of interferons, where IFN-α/β produced by CD11c+ cells (presumably DCs and macrophages) enhances the cross-priming activity of CD8α+ DCs thereby stimulating the generation of IFN-γ-producing CD8+ T cells and, finally, tumor rejection, is well known from the field of tumor immunoediting (Diamond et al. 2011; Fuertes et al. 2013). This evidence concerns the gene ITGAX and neoplasm.