LRIT3 is a leucine-rich repeat and immunoglobulin-like transmembrane protein essential for retinal ON-bipolar cell function. Primarily, LRIT3 mediates synaptic transmission between cone photoreceptors and ON-bipolar cells by regulating the localization of the cation channel TRPM1 at ON-bipolar cell dendritic tips 1. LRIT3 coordinates transsynaptic communication during cone synapse formation and maintenance, with a specific role in organizing synaptic contacts at cone pedicles 1. Mechanistically, LRIT3 may also facilitate fibroblast growth factor receptor 1 (FGFR1) trafficking from the endoplasmic reticulum to the Golgi, acting as an FGFR modulator 2. Clinically, LRIT3 mutations cause complete congenital stationary night blindness (cCSNB), characterized by selective ON-pathway dysfunction with preserved OFF-bipolar cell responses 1. LRIT3-associated cCSNB accounts for approximately 3% of cCSNB cases in some populations 3. Notably, cCSNB patients with LRIT3 mutations frequently develop high myopia, establishing LRIT3 as part of a disease mechanism linking retinal signaling defects to myopic refractive error 4. Recent therapeutic advances demonstrate that AAV gene therapy specifically targeting ON-bipolar cells can stably reverse LRIT3-deficiency phenotypes, including night vision restoration 5, representing a promising clinical intervention strategy.