In a mouse model of sarcoma, it has been shown that monoclonal antibody blockade of CTLA-4, PD-1, or PD-L1 augments glucose availability in the TME and glycolytic metabolism in T cells by restoring mTOR-mediated signaling, as well as the activity of the enzyme glutamate dehydrogenase (Glud1). The gene discussed is CTLA4; the disease is sarcoma.