The gain control of photoreceptors is largely mediated by changes in the intracellular Ca²⁺-level, which decreases as the cation channels in the receptor outer segment close in response to light. Through Ca²⁺ sensing proteins, this accelerates the recovery of the light response - lowering its overall gain - as a feedback to increased photon catch. Of these proteins, GCAPs accelerate rod and cone impulse response recovery, extending the cells' dynamic range and setting their steady-state kinetics. Recoverin is known to control photoreceptor gain at least in rods, presumably by modulating the life-time of the active photopigment. We show that recoverin controls response recovery in mammalian cones as well, studying pharmacologically isolated photoreceptor light responses recorded by ERG across isolated retinas of wild type, GCAPs-/-, and recoverin -/- mice. We also confirm the calcium-dependence of the recoverin-mediated feedback. This distinguishes its molecular target from that setting the dominant time constant of saturated light response recovery, as the latter was not found to be dependent on calcium or light in either rods or cones.