Recently, there is growing evidence, however, that NETs also can be induced by tumors through the secretion of varied tumor- and infection-derived molecules, encompassing the overexpression of granulocyte colony-stimulating factor (G-CSF) generally observed in cancer and nicotinamide phosphoribosyl transferase (NAMPT), thereby playing pro-tumorigenic roles in the scenario of cancer-associated inflammation in the majority but not all conditions (33, 34). This evidence concerns the gene CSF3 and infection.