Classically, IFNg targets monocytes or macrophages and promotes their activation to the antitumoral M1 phenotype, whereas cancer cells promote myeloid cell infiltration and (re)program macrophages towards the tumor-supporting M2 phenotype [21]; however, several studies have indicated possible protumorigenic effects of IFNg through the induction of genomic instability (e.g., copy number alterations) or an immunoevasive gene expression signature in cancer cells (PD-L1, PD-L2, CTLA-4, nonclassical MHC class Ib antigens, IDO1, etc.), which correlated with clinical observations [22]. This evidence concerns the gene IFNG and neoplasm.