Together, our data may suggest an IgE-mediated shift towards pro-inflammatory monocyte and macrophage phenotypes and may signify reciprocal monocyte-mediated activation of anti-tumor immunity such as via T cell co-stimulation and priming, a notion supported by activation of antigen presentation pathways in the tumors of mice treated with CSPG4 IgE. This evidence concerns the gene IGHE and neoplasm.