The administration of doxorubicin induces interferon γ (IFN-γ) production by CTLs, which influences the therapeutic effect, and IL-17 production by γδ T cells, which promoted CTL accumulation in the tumor bed in a mouse model of breast cancer, suggesting that γδ T cells play an important role in doxorubicin-induced antitumor immunity [20]. This evidence concerns the gene IL17A and breast carcinoma.