Studies that were initiated in experimental models and recently extended to patients suffering from melanoma showed that blockage of FOXP3+ T cells function by blocking the interaction between immunosuppressive receptor programmed cell death-1 (PD-1) largely expressed on FOXp3+ T cells and its target coreceptor on antigen presenting cells (PDL-1) using anti-PD1 mAb (nivolumab) (75) or anti-PDL-1 mAb (76) suppressed the function of tumor infiltrating Tregs, and thereby enhanced antitumor immunity to suppress tumor development and progression (75, 76). The gene discussed is FOXP3; the disease is neoplasm.