For example, knock-down of MBNL1 in unaffected mice results in a DM1-like phenotype [22], while exogenous MBNL1 overexpression in DM1 mice, likely exceeding the sequestration capacity of the foci, corrects splicing defects and related symptoms [23]. The gene discussed is MBNL1; the disease is myotonic dystrophy type 1.