This metabolic reprogramming is consistently more evident in tumor-infiltrating MDSCs as compared to circulating MDSCs, both in mouse models and human patients, and is characterized by increased CD36-mediated fatty acid uptake and higher expression of key enzymes (e.g., CPT1a, ACADM, HADHA, PGC1β), that in turn upregulate the rate of FAO necessary for the production of immunosuppressive ARG1 and cytokines driving MDSCs’ expansion (G-CSF, GM-CSF, IL-1β, IL-6 and IL-10) [165]. The gene discussed is IL1B; the disease is neoplasm.