FXN and Friedreich ataxia: Frataxin-deficient dorsal root ganglia sensory neurons produced an increase in intracellular free Ca2+ following its reduction, leading to caspase activation, increased nitrosation, and activation of pro-apoptotic gene Bax activation—events observed in FRDA patients as fragmentation of alpha-fodrin, axonal degeneration, and eventual apoptosis of these neurons, as seen through altered calcium homeostasis and cell death.