Inhibition of M2 polarization could be achieved by: (i) targeting signaling pathways such as NF-κB and STAT3 [72], (ii) treating with drugs such as all-trans retinoic acid (ATRA) that, in other tumor models, inhibit M2 polarization [73], (iii) modifying the redox machinery using association of Auranofin and Vitamin C (two commonly available drugs) that, in a preclinical model, efficiently affected multiple redox pathways [74] or silenced the ID4 molecule. The gene discussed is NFKB1; the disease is neoplasm.