Furthermore, they showed this recruitment of MDSCs is regulated by a complement-dependent pathway, complement C5a receptor 1–MDSC (C5aR1–MDSC) axis, and, when pharmacologically blocked, pro-angiogenic factors were reduced, vascular density diminished, anti-tumour immunity improved, and ultimately metastatic burden was lessened131. The gene discussed is C5AR1; the disease is neoplasm.