Interestingly, studies by several groups examining the rd7 mutant mouse line, a model for the human disease enhanced S-cone syndrome (ESCS), demonstrate that knocking out the rod-specific nuclear receptor Nr2e3, which works in concert with the transcription factor Nrl, suppresses expression of cone-specific genes in developing rods and results in a “hybrid” photoreceptor type with both rod and cone morphologic and molecular characteristics (Chen et al., 2005; Corbo and Cepko, 2005; Peng et al., 2005). This evidence concerns the gene NR2E3 and enhanced S-cone syndrome.