PKC inhibitors, reversing CELF1 hyperphosphorylation and upregulation, were shown to rescue some CELF1-dependent splicing defects in DM1 patient-derived fibroblast and myoblast cell lines [160], and to improve contractile dysfunction and mortality in the heart-specific EpA960 mouse model [161]. The gene discussed is CELF1; the disease is myotonic dystrophy type 1.