One hypothesis is that when a tumour forms near an emphysematous or inflammatory lesion, the surrounding inflammation, including numerous cytokines (interleukin-6, tumour necrosis factor-α and interleukin-1b) [46] and chemokines (CXCL8 and CXCL1), alters the autocrine and paracrine interactions between malignant cells and invading leukocytes. The gene discussed is IL6; the disease is neoplasm.