Notably, the sterile neuroinflammation in relapse–remitting MS may lead to secondary axonal damage that is caused by the redistribution of neuronal ion channels such as transient receptor potential cation channel subfamily M member 4 (TRPM4) leading to ion disbalances and glutamate-mediated excitotoxicity [95,96]. The gene discussed is TRPM4; the disease is myeloid sarcoma.