The disruption of the normal pre-miR-1 processing by MBNL1 loss of function results in increased levels of miR-1 targets, including the calcium channel CACNA1C and the gap-junction channel GJA1, which may contribute to the cardiac defects in DM1 (Rau et al., 2011). Here, MBNL1 is linked to myotonic dystrophy type 1.