When the glucose availability of CD8+ T cells is low, a short-chain saturated fatty acid called acetate participates in the synthesis of acetyl-CoA under the catalysis of acetyl-CoA synthetase, thereby enhancing metabolism to maintain the supply of acetyl-CoA, which is an important intermediate product of energy metabolism, ultimately promoting CD8+ T cell proliferation and effector function in preclinical breast cancer models [316]. This evidence concerns the gene CD8A and breast carcinoma.