Friedreich ataxia is a hereditary disease caused by mutation of the frataxin (FXN) gene and resultant low levels of the FXN protein. In a mouse model of the disease, Tomassini et al. found that subcutaneous injections of interferon-γ for 14 weeks restored FXN levels in dorsal root ganglion neurons, which are particularly vulnerable in this disease, and improved motor coordination. The findings open therapeutic avenues for Friedreich ataxia, a disease for which no specific treatments are currently available.