Also, it was shown that the endoplasmic reticulum (ER)-UPR, a known mechanism of apoptosis secondary to an overwhelming accumulation of misfolded protein [68], is involved in photoreceptor degeneration caused by missense mutations in TULP1 [69], which are associated with two forms of IRDs, early-onset retinitis pigmentosa (RP) and Leber congenital amaurosis (LCA). This evidence concerns the gene TULP1 and respiratory distress syndrome in premature infants.