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G.BodmannC

doi: 10.1146/annurev-pathol-020117-043854

In summary, while in vitro and in vivo animal studies provide evidence that SLC27A family members are likely to play a central role in FA and PUFA uptake by the RPE, we do not have a clear understanding of the retinal disease phenotypes that might occur as a result of PUFA imbalance due to SLC27A16 variation in humans