Reducing the recruitment of TAMs or reprogramming M2-like TAMs towards an anticancer M1 phenotype [13] seems a reasonable strategy to reverse immunosuppression, as well as to deal with anti-VEGF resistance, especially in glioblastoma were increased TAMs have been correlated with poor prognosis and disease progress on bevacizumab [194,195,196]. The gene discussed is VEGFA; the disease is glioblastoma.