NYX (nyctalopin) is an X-linked gene encoding a leucine-rich repeat (LRR) protein essential for normal vision, particularly in low-light conditions. The protein functions as a critical scaffold factor required for light-induced depolarization of retinal ON-bipolar cells 1, likely acting as an organizer for TRPM1 ion channels and GRM6 signaling receptors. NYX is specifically required for proper trafficking of TRPM1 to dendritic tips of ON-bipolar cells, where these channels mediate the cellular responses necessary for dim-light vision. The gene is expressed throughout retinal development and primarily localizes to the inner nuclear and ganglion cell layers, indicating its role in inner retinal circuitry 1. NYX mutations cause complete congenital stationary night blindness (CSNB1), an X-linked recessive condition characterized by severe impairment of night vision 2. This non-progressive disorder results from loss-of-function mutations that disrupt the normal visual signaling cascade in the inner retina. NYX represents approximately 3% of inherited retinal dystrophy cases in clinical cohorts 3 and has been identified as a candidate gene in early-onset high myopia families 4. As an X-linked disease arising from loss-of-function mechanisms, NYX mutations represent potential candidates for future gene replacement therapeutic strategies 2.