In line with these observations, we and others have previously demonstrated that elevated IFN signaling, resulting in the activation of ISGF3 (P-ISGF3), correlates with “hot” tumors harboring elevated numbers of tumor-infiltrating lymphocytes, active immune surveillance, repression of Mes/CSC properties, and improved therapeutic responses and outcomes [9, 12]. This evidence concerns the gene IFNA1 and neoplasm.