Due to the high genetic heterogenicity of IRDs, the disease mechanism for many of its forms is still unclear, especially for genes that have ubiquitous expression but a very specific retinal phenotype, such as the splicing factor genes, PRPF3 and PRPF8 [14,15], or NMNAT1, which encodes Nicotinamide Mononucleotide Adenylyltransferase 1, an enzyme crucial for biosynthesis of NAD+ (Nicotinamide Adenine Dinucleotide) in the cell nucleus [16,17,18,19]. This evidence concerns the gene PRPF3 and respiratory distress syndrome in premature infants.