Our null Ins finding aligns with glaucoma-specific astrocyte pathophysiology: Early-stage IOP stress: Transient Ins depletion occurs as Müller cells consume inositol for osmotic compensation against glutamate excitotoxicity; End-stage glial exhaustion: Chronic oxidative stress inactivates sodium-myo-inositol cotransporters (SMIT1), limiting Ins accumulation despite persistent osmotic imbalance. This evidence concerns the gene SLC5A3 and glaucoma.