PRCD (photoreceptor disc component) is a small ~6 kDa integral membrane protein exclusively localized to photoreceptor outer segment disc membranes 1. PRCD functions as a rhodopsin-binding protein 1 and is required for proper disc morphogenesis and rhodopsin packaging. Loss of PRCD results in disoriented disc membranes with reduced rhodopsin incorporation and decreased packing density 2. PRCD localization depends on interactions with TULP1 and TUB proteins, which mediate vesicular trafficking to outer segments 3. Mutations in PRCD cause retinitis pigmentosa (RP36), a progressive photoreceptor degeneration 4. PRCD deficiency leads to progressive rod-cone degeneration characterized by reduced visual function and slow photoreceptor death 2. Beyond photoreceptor dysfunction, PRCD deficiency triggers dysregulation of retinal cholesterol homeostasis, with 5-fold increases in cholesteryl esters and aberrant lipid accumulation 5. This precipitates retinal pigment epithelium (RPE) dysfunction including impaired phagocytosis, lipofuscin accumulation, and Bruch's membrane deposits, phenotypically resembling age-related macular degeneration 5. The progressive RPE pathology likely exacerbates vision loss during disease progression. PRCD mutations represent a distinct genetic cause of RP 6, affecting multiple species including humans and canines.