The complementarity of these two frataxin-deficient models, unicellular and multicellular, allowed the identification with an improved selectivity of 6 new compounds with high specific activity in both paradigms, one of them also active in improving heart functions in Drosophila with reduced frataxin expression in cardiomyocytes, bringing significant progress towards perspectives in FA therapy. This evidence concerns the gene FXN and Friedreich ataxia.