Glaucoma is a leading cause of blindness worldwide.1 Although it is traditionally managed as a pressure-related disease, retinal ganglion cell (RGC) degeneration can continue despite substantial reductions in intraocular pressure. This has intensified interest in the intrinsic mechanisms that determine RGC vulnerability and resilience. Among these, mitochondrial dysfunction and metabolic insufficiency have emerged as particularly compelling therapeutic targets. RGCs have exceptional energetic requirements imposed by maintenance of long axons, action-potential propagation, axonal transport, and synaptic activity.