In glioblastoma, mechanistic studies demonstrate that galectin activity intersects with several critical signalling axes, including Ras–MAPK-driven proliferation, NF-κB-mediated inflammation, hypoxia-induced HIF-1α responses, and TIM-3/PD-1-dependent immune evasion, highlighting their role in integrating extracellular cues with intracellular survival pathways. The gene discussed is HAVCR2; the disease is glioblastoma.