A recent report describes an alternative RNA-binding-protein-mediated strategy to disrupt the MBNL1 interaction with CUG repeats: a truncated MBNL1 (MBNL1∆) protein maintaining CUG-repeat binding but lacking the C-terminal domain that is implicated in splicing activity, cellular localization and oligomerization, was expressed in DM1 patient-derived cells and in HSALR mice and led to the long-lasting correction of molecular and phenotypical DM1-associated alterations. The gene discussed is MBNL1; the disease is myotonic dystrophy type 1.