Using antisense oligonucleotides against NBS1 gene, Salewsky et al [153] enforce alternative splicing of NBS1 gene in NBS patient cells and generate an internally deleted p80-nibrin protein, which skips the mutated exon, carries both amino terminal and carboxyl terminal domains, and possesses undisguisable DNA replication characteristics compared with control NBS1 protein. The gene discussed is NBN; the disease is Nijmegen breakage syndrome.