Considering that frataxin directly interacts with ITPR1 and that accumulation of LDs and increased lipogenesis have been previously described in fibroblasts of FRDA patients, cardiomyocytes of mice and glial cells of Drosophila [446–448], it is conceivable that ITPR1-mediated signals may contribute to frataxin deficiency-triggered lipid dyshomeostasis together with other mechanisms [449, 450], which probably also occur in Purkinje and other cerebellar cells. Here, ITPR1 is linked to Friedreich ataxia.