A number of alternative exons, such as GRIN1 exon 4, APP exon 7, and Tau exons 3 and 9, which have already been reported to be mis-spliced in the brains of DM1 patients, were unaltered in Mbnl1–/– mice, thus indicating a limited contribution of MBNL1 to DM1 CNS defects (Suenaga et al., 2012). The gene discussed is MBNL1; the disease is myotonic dystrophy type 1.