Furthermore, the ability to recapitulate the difference in autofluorescence material accumulation between control and CLN3 disease hiPSC-RPE cells after prolonged exposure to unaffected (no CLN3 mutation) POS, suggests that RPE autonomous CLN3 dysfunction is sufficient to instigate the reduced RPE autofluorescence observed in CLN3 disease eyes. This evidence concerns the gene CLN3 and glycogen storage disease VI.