OSM and neoplasm: Tumor-associated neutrophils can favor genetic instability via the release of ROS, promote tumor cell proliferation via elastase, sustain angiogenesis via the release of vascular endothelial growth factor (VEGF), enhance neoplastic cell invasiveness by secreting hepatocyte growth factor (HGF), oncostatin M (OSM)[43], and matrix metallopeptidase 9 (MMP-9), and suppress effective antitumor CD8+ T cell immunity via arginase expression[44].