Given the dual mechanism of LGMN for regulating macrophage infiltration and GBM cell proliferation through activating GSK3β/STAT3 and integrin αv/AKT/p65 signaling, respectively, we explored the impact of cotargeting macrophages (using the GSK3β inhibitor AR-A014418 or the STAT3 inhibitor WP1066) and GBM cells (using the integrin αv inhibitor cilengitide) in mouse models. The gene discussed is STAT3; the disease is glioblastoma.