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Screening and development of small molecules to inhibit the binding sites of the two proteins are topical not only in the context of FRDA but also in other neurodegenerative and inflammatory diseases (reviewed in Combating repressive chromatin marks and epigenetic FXN silencing, histone deacetylase inhibitor 109/RG2833 treatment in a neuronal cell model increases both FXN mRNA and protein levels concomitant with increased H3K9 acetylation in patient clinical trials (Soragni et al., 2014)
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