The light-rise of the electrooculogram is believed to originate from a substance released from the rods after dark adaptation. The identity of this "elusive" light-rise substance has not been demonstrated, and therefore a new perspective on the light-rise is presented. The light-rise is caused by the depolarization of the basolateral membrane of the retinal pigment epithelium (RPE) has become clearer in the last decade with the identification of calcium as the intracellular secondary messenger and the role of bestrophin as a regulator of intracellular stores of calcium and controlling the cytosolic calcium levels through L-type calcium channels. The light-rise depends upon a change from darkness to light, which triggers the intracellular cascade resulting in the depolarization of the basolateral membrane. The same intracellular signaling molecules, notably calcium and inositol triphosphate (IP3), are strongly implicated in this cascade. Recent studies have now led to a clearer understanding of the roles and functions of the ion channels and their contribution to the light-rise with IP3 regulating the release of calcium for intracellular stores. Given that calcium and IP3 are also regulators of phagocytosis, and that the initiation of rod outer segment phagocytosis is initiated with lightonset, it may be that the light-rise is generated in response to this physiological event. Therefore, the putative light-rise substance may not be released by the rods, but follow directly from IP3 release from the RPE's phospholipid membrane following the onset of light and the initiation of phagocytosis. The light rise substance, could be considered to be light itself.