The block of S100B action using PTM, which is regarded to inhibit the interaction between the protein and the transcription factor p53 [41], likewise results in the amelioration of clinical, neuropathological, and biomolecular parameters in animal models of relapsing remitting MS in EAE SJL mice, as indicated in [13]. The gene discussed is S100B; the disease is relapsing-remitting multiple sclerosis.