CXCL8, CXCL5, and CCL2, together with other stimuli, such as lipopolysaccharide (LPS) and IFNβ, or the inhibition of TGFβR signaling, enhance the oxidative burst in neutrophils and the consequent production of H2O2 which activates a signaling cascade in tumor cells, leading to TRPM2 activation and cell injury up to death due to a lethal influx of calcium (Ca2+) [91,128]. The gene discussed is CXCL5; the disease is neoplasm.