At sites of cancer and inflammation, the exposure to cytokines such as the interleukin 1β (IL1β) and granulocyte-colony-stimulating factor (G-CSF) and the recognition of neutrophil pattern recognition receptors (PRR) by damage-associated molecular patterns (DAMP) and pathogen-associated molecular patterns (PAMP) increase the neutrophil lifespan dramatically through inhibition of apoptosis [29]. Here, CSF3 is linked to cancer.