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In two patients with complex I deficiency associated myopathy, complex I activity has been normalized upon riboflavin therapy with an evident clinical improvement ( ACAD9 is involved in complex I function, deficiency state, and responsiveness to riboflavin ( in vitro ( ETFDH ) gene mutations, riboflavin therapy can lead to clinical improvements ( Riboflavin Ameliorates Neuroinflammation Riboflavin has the ability to suppress nuclear factor-kappaB (NF-B) activity exerting an anti-inflammatory property

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