For example, in melanoma, a type I IFN signature correlated with CD8+ T cell infiltration and IFNβ production by tumor-associated DCs has been shown to be critical for mediating antitumor immunity 124 This function may prove to be particularly useful for the so-called cold tumors, which, in response to β-catenin signaling, lack the production of CCL4 and fail to recruit CD103+ DCs and produce IFNβ within the tumor microenvironment and, consequently, are deprived of the CXCL9/10 chemokines that drive T cell influx 125. This evidence concerns the gene IFNB1 and melanoma.