As such, our finding that the CD28-ARS2-PKM2 axis endows the metabolic flexibility needed for optimal CD8+ T-cell-mediated antitumor immunity in mice is consistent with recent reports demonstrating that CD28-stimulated glucose metabolism enhances effector properties and the checkpoint blockade response of tumor-infiltrating T cells in cancer patients [63, 64, 67]. This evidence concerns the gene CD28 and neoplasm.