POLR3A and Friedreich ataxia: Indeed, in protein–protein interaction networks proposed by Synofzik and Schüle, the proteins encoded by POLR3A and FXN, as the causative gene of Friedreich's ataxia, were shown to cluster in the same highly connected “protein community.”24 It is possible, for example, that the proteins and metabolic pathways affected by these two diseases encompass a common element involved in mitochondrial function.