In patients with IgM anti-MAG neuropathy, RTX mitigated pain and paresthesia through T reg cell activation (Dalakas et al., 2009), and in patients with multiple sclerosis, B-cell depletion caused inactivation of Th-cell activity in an autoantibody-independent manner (Stuve et al., 2005). This evidence concerns the gene CD40LG and neuropathy.