As a result, researchers hypothesized that inhibiting the CTLA4-B7 interaction would lead to increased and extended T-cell activation, as evaluated by the higher release of IL-2, IFN-γ, IL-3, IL-4, IL-5, and IL-10, as well as more clinically relevant anti-tumor immune responses [44–46]. The gene discussed is IFNG; the disease is neoplasm.