FXN and Friedreich ataxia: In human iPSC-based studies of FRDA, which is caused by an intronic repeat expansion in the FXN gene encoding Frataxin, disease-relevant phenotypes such as reduced Frataxin mRNA and protein levels as well as mitochondrial defects were observed in cardiomyocytes and peripheral sensory neurons, two of the affected cell types in FRDA33–36.