For example, persistent inflammation is able to induce NF-κB activation in renal cancer cells,121 which, on a background of genetically activated HIF2A signalling, can lead to the expression of mediators of metastasis.116,121 Enhanced inflammatory signalling through NF-κB can also modulate Wnt signalling in CRC, highlighting the general relevance of inflammation as a modulator of oncogenic signal output.122. The gene discussed is EPAS1; the disease is renal carcinoma.