Recently, a group in UT Southwestern used CRISPR/Cas9 with single-guide RNAs to destroy the conserved splice acceptor or donor sites preceding DMD mutations or to bypass mutant or out-of-frame exons, thereby allowing splicing between surrounding exons to recreate in-frame dystrophin proteins lacking the mutations and was able to rescue dystrophin function in up to 60% of DMD patients [151]. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.