An inflammatory phenotype has been demonstrated to characterize TAMs in many tumors16, and inflammation stimulates carcinogenesis through multiple pathways: excretion of epidermal growth factor, proangiogenic signals such as VEGF and fibroblast growth factor 2, several proinflammatory cytokines and chemokines, and factors such as matrix-degrading enzymes, metalloproteinases, cysteine cathepsin proteases, and heparanases all contribute to a tumor-promoting environment.17,18. This evidence concerns the gene HPSE and neoplasm.