Recently, it has been suggested that IL-6, which is derived from cancer cells as well as from tumor stromal cells, such as cancer-associated fibroblasts and infiltrating immune cells [7, 33], may modulate both the local tumor microenvironment and the chronic systemic inflammatory response by causing the differentiation of tumor-infiltrating monocytes into immunosuppressive, M2-like macrophages [34] and by attracting regulatory T cells [35] in patients with cancer, thereby allowing cancer cells to acquire an advanced malignant phenotype. This evidence concerns the gene IL6 and neoplasm.