These contrasting results and historic setbacks in targeting TNF in MS patients have since been attributed to distinct TNF activities mediated by interactions of soluble (s)TNF and its transmembrane (tm)TNF precursor with their preferential TNFR1 and TNFR2 receptors: sTNF with higher affinity for TNFR1 mediates apoptosis and chronic inflammation [17]. This evidence concerns the gene TNF and myeloid sarcoma.