Background <p>T-cell metabolism is targeted by cancer cells in an attempt to escape immune surveillance. The mitochondrial branched-chain aminotransferase, BCATm, is overexpressed in cancer, yet its role in T-cell immunity is suggested but understudied.</p> Methods <p>C57BL/6 mice with T-cell specific-single BCATm deficiency were used to determine the impact of BCATm on T-cell function in vitro and in vivo using the murine EL4-OVA lymphoma. The studies were complemented by a transcriptomic correlation analysis of BCATm in human T cells and by using siRNA to knock-down BCATm in Jurkat T cells.</p> Results <p>The loss of BCATm from CD4⁺ T cells increased mitochondrial respiration but reduced the coupling between oxygen consumption and ATP synthesis, redirecting the cells to glycolysis. This compensation sustained T-cell functionality as seen by increased release of IFN-γ from CD4⁺ T cells or granzyme B and perforin from CD8⁺ T cells. Human studies further suggested that BCATm negatively affected T-cell mitochondria. While EL4-OVA tumours from T-BCATm^KO mice were enriched in memory precursor CD4⁺ and CD8⁺ T cells, reduced EL4-OVA lymphoma growth was achieved in mice with T cells carrying a combined deletion of BCATm and BCATc.</p> Conclusions <p>BCATm is an immunosuppressive enzyme that may weaken T-cell performance in the lymphoma microenvironment.</p>