Immunometabolism has emerged as a hot topic because of its central role in immune control. T cells undergo substantial metabolic changes during activation, which allows them to mediate effector responses. While chimeric antigen receptor T cell-adoptive treatment has demonstrated remarkable clinical efficacy, it has not been able to successfully induce a robust antitumor response in many individuals. Solid tumors provide stiff competition by producing a hypoxic and glucosuric microenvironment that saps the energy of T cells and drives them to exhaustion. However, other inherent features of T cells, including durability, lifespan, and functioning, all play crucial roles in determining the efficiency of immunotherapy. T cells are key mediators of tumor death, and their specificity for tumor-expressed antigens is of paramount relevance. The pathways of cellular signaling and epigenetics are not the only ones influenced by metabolic activity, which has a significant impact on the trajectories of T cell development and fate. In addition, T cell “exhaustion” and CAR-T cell efficiency can be compromised by the immunosuppressive tumor microenvironment (TME), which is characterized by acidity, hypoxia, nutritional depletion, and metabolite buildup due to the high metabolic demands of tumor cells. Cancer cells’ metabolism is altered by hypoxia, and the resulting cellular quiescence adds to resistance to treatment. This chapter summarizes how the tumor microenvironment (TME) might affect the metabolic pathways of T cells at various stages of development. To further the practical use of CAR-T cell therapy, we also propose potential metabolic techniques to enhance the efficiency and longevity of CAR-T cells.