Inspired by a recent study that systematically addressed the optimal design of LNA-based SSOs targeting the human dystrophin exon 58 sequence [29], here we designed a series of LNA-modified antisense oligonucleotides and evaluated their ability to induce skipping of the dystrophin exon 51 in myoblast cells derived from a DMD patient. Here, DMD is linked to Duchenne muscular dystrophy.