At the metabolic–innate checkpoint intersection, glioblastoma increases fatty-acid oxidation and upregulates CD47, creating phagocytosis-proof tumor cells; phagocytic checkpoints on TAMs can be overcome only when innate signals are combined with genotoxic or STING agonism, aligning LR maps with actionable dependencies (55, 56). The gene discussed is CD47; the disease is glioblastoma.