Since we showed that the phosphorylation status of PKM2 in rodent retina decreases after experimental retinal detachment to increase catabolic activity, the metabolic reprogramming observed in the retina of the Pkm2−/− mice may mimic this activation of PKM2 by substituting constitutively active PKM1 to circumvent acute apoptotic stress and ultimately, improve photoreceptor survival. Here, PKM is linked to retinal detachment.