However, in vitro and in vivo models of MS have linked an increased axonal expression of CNTN1 to the signaling pathways involved in remyelination.34,35 Consequently, lower levels of CNTN1 in CSF and serum could be a consequence of active retention of CNTN1 into axons to support myelination and axonal repair and, therefore, reflect a restorative mechanism. The gene discussed is CNTN1; the disease is myeloid sarcoma.