MDSC are considered a major cellular contributor of the suppressive TME [141,142], and tumor-associated growth factors such as granulocyte–macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), and signaling pathways such as STAT3 and STAT5 are known to upregulate lipid transport receptors (such as CD36 and Msr1) in MDSC and enhance lipid accumulation [123]. This evidence concerns the gene CSF3 and neoplasm.