MBNL1 and myotonic dystrophy type 1: These results are in agreement with previous studies performed in cortical astrocytes of the DMSXL mouse and brain samples of affected humans [14,30]; demonstrating that in MIO-M1 DM1 cells, even lacking the DMPK genomic context, the CTG expansion is still able to recapitulate many molecular features of the disease, including splicing defects and accumulation of RNA foci colocalized with MBNL proteins.