The development of an RPE-specific inducible Prom1-KO mouse model would be particularly valuable, as it would enable in vivo testing of whether Prom1 loss alone drives mitochondrial failure, autophagy impairment, junctional instability, partial EMT, and cell-autonomous RPE degeneration through similar transcriptomic changes—phenocopying key pathogenic mechanisms shared between aAMD and IRDs. The gene discussed is PROM1; the disease is respiratory distress syndrome in premature infants.