In light of the prominent expression of RanBP2 and HKI in retinal neurons [1,19], the vital dependence of the neuronal retina (and brain) on glucose as the main substrate source for energy production, and the determinant impact of metabolic disorders, such as diabetes, in retinal function (e.g., diabetic retinopathy) [37], we probed the impact of deficits in RanBP2, HKI, and ATP, on the electrophysiological responses of subclasses (rod and cone) photoreceptor and postreceptor retinal neurons of RanBP2+/− and in RanBP2+/+ mice. This evidence concerns the gene RANBP2 and metabolic disease.