For this reason, new therapies have focused on both targeting the blockade of IL4Rα in TAMs [52] and on the suppression of M2 polarization to enhance M1 macrophage activity, for example, by blockade of IL4Rα in TAMs along with administration of zoledronic acid, induced apoptosis and delayed breast tumor progression [19,53]. The gene discussed is IL4R; the disease is breast neoplasm.