An internally truncated form of γ-sarcoglycan can substitute for the full-length protein, according to new research published in The Journal of Clinical Investigation. Gao et al. used an exon-skipping approach to bypass a frameshift mutation in the γ-sarcoglycan (SGCG) gene that causes limb-girdle muscular dystrophy. The resulting protein, termed Mini-Gamma, rescued γ-sarcoglycan deficiency in transgenic flies and mice. The researchers also demonstrated induction of exon skipping in human cells carrying SGCG mutations, implying that exon skipping could be a viable therapeutic approach in patients with limb-girdle muscular dystrophy.