Cancers drive the expansion of heterogeneous immature myeloid cells [8,9] through elicitation of tumor-derived factors (TDFs), including growth stimulating factors (e.g., CSFs), cytokines (e.g., IL-10, IL-6, IL-4, IL-8) and prostaglandins; these act in a paracrine and/or systemic fashion to sculpt a pro-tumor microenvironment [29] and to guide the pathological differentiation of myeloid lineage into alternatively activated and immunosuppressive cells, mainly represented by tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) [30]. The gene discussed is IL6; the disease is neoplasm.