Right from tumourigenesis, IL-17 has been shown to play a role via combination of releasing MDSCs to dampen the body's immune defence system, as well as stimulating proinflammatory cytokines systemically (via the NF-κB pathway) and locally (via CCL2) to maintain an inflammatory environment, resulting in the stimulation of tumour growth via the subsequent expression of antiapoptotic genes and the consequent increased survival of cells with protumourigenic potential. Here, NFKB1 is linked to neoplasm.