Broadly, two strategies have been investigated in pre-clinical models: depletion of myeloid cell numbers (via blockade of CCL2/CCR2, M-CSF/M-CSF receptor, and VEGF/VEGF receptor) and manipulation of myeloid cell function/plasticity (introduction of anti-cancer cytokines to TME, inhibition of STAT3 signaling, triggering toll-like receptors 3 and 9, and inhibiting CD36, inducible nitric oxide synthase, arginase-1, and indoleamine 2,3 deoxygenase) [113]. The gene discussed is CCL2; the disease is cancer.