Neutrophils can promote invasion via release of proteases and neutrophil extracellular traps and by sustaining IL-6/STAT3 and NF-κB signaling; circulating monocytes differentiate toward tumor-associated macrophages that support angiogenesis, extracellular-matrix remodeling, and immune evasion; conversely, lymphopenia reflects impaired anti-tumor surveillance (19, 20). The gene discussed is STAT3; the disease is neoplasm.