Intron retention typically occurs in G/C-rich, autosomal dominant expansion diseases (such as DM, Fuch’s endothelial corneal dystrophy, and C9orf72), but not in A/T-rich expansion diseases (such as Friedreich ataxia and SCA10); it has a wide cellular impact on tissue development, neuronal gene expression, RNA nuclear retention, and nucleocytoplasmic transport, to name but a few [52]. This evidence concerns the gene C9orf72 and spinocerebellar ataxia type 10.