We subsequently published proof-of-concept studies demonstrating that increasing systemic TLR2 tolerance by administering low-dose exogenous L654 or Pam2CSK4 (P2C; a commercially available TLR2 agonist) to mice resulted in the following: (1) significant attenuation of disease severity in a model of MS, experimental autoimmune encephalomyelitis (EAE) (17); and (2) significant enhancement in murine central nervous system remyelination following cuprizone-mediated demyelination (18). The gene discussed is TLR2; the disease is myeloid sarcoma.