Considering that one of the known effects of IL-4, characteristic of Th2 cells, is the polarization of M2 macrophages, which reciprocally promote the response of the first through release of CCL17 and CCL22 chemokines [17], increased circulating IL-4 could merely constitute a reflex of what occurs in the tumor microenvironment with respect to the possible infiltration of suppressor profile TAMs, induced by Th2 lymphocytes, as well as by the tumor itself. The gene discussed is CCL17; the disease is neoplasm.