Adoptive T-cell therapy (ACT) of cancer， which involves the infusion of -engineered tumor epitope reactive autologous T cells into the tumor-bearing host， is a potential treatment modality for cancer. However， the durable antitumor response following ACT is hampered either by loss of effector function or survival of the antitumor T cells. Therefore， strategies to improve the persistence and sustain the effector function of the antitumor T cells are of immense importance. Given the role of metabolism in determining the therapeutic efficacy of T cells， we hypothesize that inhibition of PIM kinases， a family of serine/threonine kinase that promote cell-cycle transition， cell growth， and regulate mTORC1 activity， can improve the potency of T cells in controlling tumor.