While exon-skipping to correct out-of-frame mutations has been used successfully to treat dystrophin-deficiency (Duchenne dystrophy), it seems problematic for laminin-deficiency in that skipping of nearly all LAMA2 exons will result in either cysteine mispairing with improper domain folding and disulfide-bond formation and/or major loss of functional domains. The gene discussed is DMD; the disease is hyperinsulinemic hypoglycemia, familial, 4.