A team led by investigators at the University of Rochester in New York this week show that "nuclear-retained transcripts containing expanded CUG-CUG^exp — repeats are unusually sensitive to antisense silencing," and that, in a transgenic mouse model of myotonic dystrophy type 1, the systematic administration of antisense oligonucleotides causes "a rapid knockdown of CUG^expRNA in skeletal muscle, correcting the physiological, histopathologic and transcriptomic features of the disease." Overall, as the Rochester-led team reports in Nature, "these results provide