For about two million people worldwide affected by inherited retinal degeneration, namely retinitis pigmentosa (RP), irreversible vision loss results from mutations in any of 64 genes known so far that trigger disruption of rod photoreceptor function and the metabolic and redox signaling between rod and cone photoreceptors. The cones are essential for color perception and visual acuity and die in the final phase of RP in response to the loss of rod trophic support. The restoration of this signaling by administration of rod-derived cone viability factor (RdCVF), a protein secreted by rods and necessary for the metabolic function of cones, is a promising therapeutic approach aimed at preventing broadly the loss of cone vision independently of the causative RP mutation.  The mechanisms that underlie RdCVF prevention of cone death may provide insights into metabolic changes that contribute to degenerative processes in other parts of the nervous system.