This mutation results in a novel soluble splice form of the TNF receptor (TNFR1) that, in contrast to the membrane bound form, lacks NF-κB activity and apoptotic activity but can block the function of TNF and thus mimics anti TNF therapies, which exacerbate MS (Gregory et al., 2012). This evidence concerns the gene TNFRSF1A and myeloid sarcoma.