The ASO strategy has also been successfully used for targeting the pre-mRNA to restore prematurely stopped open reading frames, such as in the inherited disease dystrophic epidermolysis bullosa (DEB) [57], induce isotype switching of the Tau mRNA in the frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) [58], generate a truncated APOB100 protein with therapeutic utility to prevent the development of atherosclerosis [59], or induce exon inclusion of the exon necessary for the treatment of cystic fibrosis [60]. Here, APOB is linked to Dystrophic epidermolysis bullosa.