In 1992, Yednock first published evidence that α4β1 integrin plays a critical role in the induction of lymphocytes to the inflamed brain, and that antibodies to α4β1 integrin or its ligand VCAM-1 blocked MS pathogenesis and inhibited the development of experimental autoimmune encephalomyelitis (EAE), the most commonly used experimental model for MS [5,27]. This evidence concerns the gene VCAM1 and experimental autoimmune encephalomyelitis.