CD68 and neoplasm: Although IgE may exhibit anti-tumor responses via activation of various effector cells, the preferential colocalization of IgE and its receptor FcεRIα with CD68+ macrophages in the tumor and increased macrophage function after treatment with sera from Prdm1fl/flFoxp3YFP-Cre tumor-bearing mice suggest that macrophages are likely major effector cells participating in the IgE-mediated anti-tumor response, in line with other reports [34, 35].