Despite those results, we had learned that, from a physiopathogenic point of view, genetic or epigenetic events could play a role to modify the course of diseases, including notch protein and signalling pathway in CADASIL and MS [3], or mitochondrial cytopathies such as Leber’s disease or POLG mutations which have been suggested to promote MS [4,5]. This evidence concerns the gene POLG and Leber congenital amaurosis.