Duchenne muscular dystrophy (dmd) is an x-linked recessive genetic disease caused by mutations in the gene that encodes dystrophin, a large protein that plays an important role in the development of normal muscle fibers. the dystrophin gene is immense, spanning 2.5 million base pairs, and includes 79 exons and 78 introns. many of the mutations that cause dmd produce premature stop codons, which bring protein synthesis to a halt, resulting in a greatly shortened and nonfunctional form of dystrophin. some geneticists have proposed treating dmd patients by introducing small rna molecules that cause the spliceosome to skip the exon containing the stop codon. the introduction of the small rnas will produce a protein that is somewhat shortened because an exon is skipped and some amino acids are missing, but it may still result in a protein that has some function. the small rnas, antisense rnas, used for exon skipping are complementary to bases in the pre-mrna, which will prevent proper associating of spliceosome for intron removal. (a. goyenvalle et al., 2004. science 306: 1796-1799). in order to skip the mutated exon and potentially treat dmd, select the best antisense rna targets. a- a 5' splice site of the intron upstream of the exon to be skippedb- a branch point of the intron upstream of the exon to be skippedc-a 5' splice site of the intron downstream of the exon to be skippedd-a 3' splice site of the intron upstream of the exon to be skippede-a 3' splice site of the intron downstream of the exon to be skipped