This includes the release of ARG-1 to create an immune-suppressed environment; MMP-9 to promote the infiltration of tumor cells and tumor angiogenesis; and other potent serine proteases, e.g., neutrophil elastase (NE), Cathepsin G, and human proteinase 3 that can shape the TME at the metastatic site. The gene discussed is PRTN3; the disease is neoplasm.