Tumour secreted factors, including HMGB1, can prime macrophages for inflammasome activation and polarise them into a pro-tumourigenic M2-like phenotype via TLR2, suggesting that TLR2 signalling is critically important for the inflammatory and polarising effects of the tumour microenvironment and that TLR2 represents a promising target to limit EAC disease progression. This evidence concerns the gene HMGB1 and neoplasm.