Firstly, targeting glucose transporters (e.g., GLUT1) via degraders [57–59], such as GLUT1-proteolysis targeting chimeras (PROTAC) to disrupt glycolytic metabolism, thereby imposing nutrient deprivation, then restoring VPS37A functionality through tumor-localized delivery systems [60–62]—such as oncolytic adenoviruses carrying hypoxia-inducible VPS37A expression cassettes, CRISPR/Cas9 ribonucleoproteins with tumor-penetrating peptide carriers for precise gene editing, or lipid nanoparticles coated with EGFR-targeting scFv antibodies encapsulating optimized VPS37A mRNA. The gene discussed is SLC2A1; the disease is neoplasm.