EOS can be recruited into the tumor microenvironment under the influence of chemokines, where they upregulate E-cadherin to inhibit cancer cell proliferation and secrete cytotoxic granules and various pro-inflammatory mediators (e.g., IL-2, IL-4, IL-5, TNF-α, TGF-β), thereby modulating T cell phenotypes and affecting tumor development (38–40). The gene discussed is IL4; the disease is neoplasm.