A team led by investigators at the University of Rochester in New York this week show that "nuclear-retained transcripts containing expanded CUG-CUGexp — 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 CUGexpRNA 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