In animal models of MS, FIB enters the CNS parenchyma via the damaged BBB, which is deposited in the form of insoluble fibrin in the brain tissue (11) and binds to the CD11b/CD18 integrin receptor, which induces ROS release in the microglia and recruitment of peripheral macrophages and T cells, leading to autoimmune demyelination and axonal destruction (14, 26–28). This evidence concerns the gene ITGAM and myeloid sarcoma.