Recently, chemically engineered antisense oligonucleotides against this miRNA, also called antagomiRs, have been described as a candidate therapy for DM1 because of their potential to upregulate endogenous levels in MBNL1 and 2, thus compensating for sequestration by expanded CUG repeat RNA. The gene discussed is MBNL1; the disease is myotonic dystrophy type 1.