Indeed, using exon-junction microarrays and RNA-Seq on hippocampal tissue, we found hundreds of alternative exons whose splicing was altered on Mbnl2 depletion in mice, suggesting that Mbnl2 loss-of-function might explain several CNS phenotypes, including hypersomnia and learning/memory deficits observed in both Mbnl2 KO mice and DM patients (35). The gene discussed is MBNL2; the disease is hypersomnia.