For example, treatment of melanoma mice with TIM‐1 antibody resulted in increased infiltration of CD4 and CD8 T cells as well as increased production of granzyme and IFN‐γ by T cells.[26] In an animal model of breast cancer, use of PD‐1 monoclonal antibody to block the PD1 – PD‐L1 interactions between B cells and tumor‐derived MDSCs attenuated the PD1+ B‐cells’ inhibitory effects on T‐cell proliferation and IFN‐γ secretion, as evidenced by reduced tumor growth.[51, 52] Thus, blocking B cell Ics restores the role of B cells in assisting T cells to exert antitumor toxic effects. The gene discussed is CD4; the disease is breast carcinoma.