While M2-type tumor-associated macrophages (TAMs) are well recognized for their immunosuppressive and tumor-promoting functions in breast cancer, M1 macrophages—classically activated by IFN-γ and microbial stimuli—exert contrasting effects by promoting antitumor immunity and reprogramming the tumor microenvironment (TME) toward a more hostile landscape for cancer progression [83, 84]. This evidence concerns the gene IFNG and neoplasm.