Ni X. et al. showed that the interaction of Gal-9 and TIM-3 on macrophages leads to increased secretion of M2-associated proangiogenic factors such as vascular endothelial growth factor VEGF-A, while blockade of Gal-9/TIM-3 signaling inhibits M2 polarization and suppresses tumor growth in glioblastoma models [75]. The gene discussed is HAVCR2; the disease is neoplasm.