Eosinophils recruitment to the tumor sites is driven by a combination of cytokines (i.e., IL-5), adhesion molecules (i.e., CD11a (LFA1), CD11b (MAC1), chemokines (CCL11, CCL24, CCL5), and VEGFs produced by tumor and immune cells as well as damage-associated molecular patterns (DAMPs) or alarmins produced by dying tumor cells, including high-mobility group box 1 protein (HMGB1), IL-1α and IL-33 that both attract eosinophils and enhance their survival and activation [22, 47, 80, 81]. This evidence concerns the gene ITGAL and neoplasm.