SLC24A1 encodes a calcium-potassium-sodium antiporter located in retinal photoreceptor outer segments that exchanges 1 calcium and 1 potassium ion for 4 sodium ions. It is a critical component of the visual transduction cascade, controlling cytosolic calcium concentration in rod and cone photoreceptors during light and darkness. Light-induced lowering of calcium in the outer segment is mediated by extrusion via SLC24A1, which plays a key role in light adaptation. Pathogenic variants in SLC24A1 cause congenital stationary night blindness (CSNB), a nonprogressive retinal disorder manifesting as impaired night vision 1. The gene exhibits a Riggs-electroretinogram phenotype characterized by normal visual acuity and absence of myopia or nystagmus 2. Recent genetic studies have expanded the phenotypic spectrum of SLC24A1 beyond CSNB; variants have been associated with autosomal recessive retinitis pigmentosa and mild retinal degeneration with marked macular involvement 3. SLC24A1 mutations account for approximately 5% of CSNB cases in Indian cohorts 4. Currently, no disease-modifying therapies specifically target SLC24A1 dysfunction; management remains supportive for this nonprogressive condition.