Based on the report that CCR2 and CCR5 are highly expressed on helper T cells and that CCL3 can attract the migration of CD4+ T cells to the site of infection [35-37], we speculate that another consequence of the drastically induced CCL3 by FusOn-H2 is the recruitment of CD4+ T cells to the tumor site, which can then secret abundant IFN-γ. The gene discussed is CD4; the disease is infection.