Using these data, we selected eight direct targets of miR-23b that were both significantly repressed or unchanged (Figure S4A) in a CNT vs. DM1 comparison, and were significantly upregulated comparing control and DM1 muscle cells treated with the corresponding antagomiR (CHUK, SRC, NOTCH2, TAB2, SIRT1, HMGB2, MET, and PLAU). This evidence concerns the gene HMGB2 and myotonic dystrophy type 1.