The depletion of extracellular glucose in the TME, as well as factors derived from tumor cells like GM-CSF in select tumor models, can cause TANs to upregulate fatty acid uptake, reprogramming them towards a phenotype of protumor TANs that suppress antigen-specific antitumor CD8+ T cells [256,257,258,259,260,261]. The gene discussed is CSF2; the disease is neoplasm.