Multiple sclerosis is certainly a complex disease entity and the pathogenic process involves more than just increased neuro-degeneration. In particular, reduced remyelination contributes to disease progression. Thus, relevant targets in addition to the HERV peptide might exist, possibly host proteins with a homology to the HERV peptide. One such candidate is neuron-specific ankyrin-2 which, owing to complementary binding sites, forms a complex with spectrin. In an animal model of remyelination of axons the latter is the target of an immune repair mechanism mediated by a monoclonal antibody [63] .