GPR143 and ocular albinism: In addition, this localization of OA1 is consistent with its proposed role as a stop signal for melanosome overgrowth during melanogenesis [6], [7] and could explain the changes in RPE phenotype observed in ocular albinism: mutations or deletions in OA1 producing a non functional OA1 protein would allow a continuous vesicular traffic of membrane proteins to melanosomes resulting in the formation of macromelanosomes [3].