FCER2 and neoplasm: Indeed, recent fascinating hypotheses give support to the notion that, in tumor, IgE via interaction with its receptors (FcεRI and CD23) can engage and re-educate alternatively-activated macrophages (TAMs) towards pro-inflammatory phenotypes and prime all subsets to mediate anti-tumor functions, finally pointing to IgE as a novel anti-cancer modality [41–43].