The second line of evidence derives from a comparison of the expression pattern of many type I genes in rd7 and Nrl −/− mutant backgrounds. As mentioned above, Nrl is a retinal transcription factor that, when mutated, results in en masse conversion of rods into S-opsin–expressing cones [24]. It can be inferred from this fact that Nrl is absolutely required for the normal silencing of cone-specific genes in rods. In the Nrl homozygous mutant, there is a stronger and more uniform derepression of many cone-specific genes throughout the ONL than is seen in the rd7 retina (unpublished data). This finding further suggests that, in addition to its repression of cone gene expression via induction of Nr2e3 expression, Nrl exerts an additional level of negative control over cone genes either directly or via a second, as yet uncharacterized, repressor.