In vivo, research with a glioblastoma mouse model demonstrated that CSF-1R blocking effectively promoted M1 polarization of MACs and suppressed glioma growth.45 Similarly, the inhibitory small molecule toosendanin was shown to induce M1 polarization in a glioblastoma mouse model.84 These findings suggest that similar mechanisms could enhance the antitumor activity of CAR-MACs. The gene discussed is CSF1R; the disease is glioblastoma.