Future studies should explore combination therapies such as immune checkpoint blockade with the hybrid A2/NY-T cells, as well as coengineering strategies like enforced proinflammatory cytokine secretion (eg, IL-12, IL-18) to rationally exploit endogenous immunity.25 41 Also to be elucidated are the molecular mechanisms behind such vast differences in in vitro function and tumor control between the different-affinity A2/NY-T cells.76 The gene discussed is IL18; the disease is neoplasm.