These pro-tumoral effects are mediated through multiple mechanisms, including angiogenesis stimulation via Vascular Endothelial Growth Factor (VEGF) secretion, facilitation of tumor cell migration, and immune suppression through the release of neutrophil elastase (NE), interleukin 8 (IL-8), and arginase-1 (ARG1) [7,8,9,10,11,12]. This evidence concerns the gene ARG1 and neoplasm.