Activated CD8+ CTLs exhibit upregulation of the glycolytic pathway and require CD28 costimulatory signaling to prolong the duration of glycolytic upregulation; in an obese mouse model of breast cancer, the knockdown of STAT3 in CD8+ CTLs or treatment with inhibitors of fatty acid oxidation increases both glycolysis and the toxic function of CD8+ CTLs (including IFN-γ, granzyme B and CD107a) and thereby inhibits mammary tumor development [148]. This evidence concerns the gene CD8A and breast cancer.