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Moreover, overlapping pathological features exist for diabetes, IR, and AD

Haploinsufficiency of the SLC52A1 (OMIM#615026) due to maternal microdeletion and heterozygous intronic variant has been reported to cause a transient riboflavin responsive neonatal multiple acyl-CoA dehydrogenase deficiency that resolved with oral supplementation of riboflavin [27-29]

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