Under the influence of glioma-derived TGFB1, GAMs demonstrate negligible anti-tumor activity and are polarized to produce pro-tumorigenic molecules.7 Moreover, through a positive feedback paracrine loop,8 GAM-derived TGFB1 promotes glioma growth9 and invasion.10 Therapeutic targeting of TGFB signaling11 and GAM recruitment12 has demonstrated survival benefits in preclinical rodent models, but these interventions have not been successful in glioma patients. Here, GLS is linked to neoplasm.