Emblematically, drug discovery focused on the role of TNF-α in NeP has been focalized either on the blockade of TNFR1 signaling (e.g., in rheumatoid arthritis) [70] or on the design of effective agonists at the TNFR2, which have been used for multiple clinical conditions such as spinal cord injury-induced locomotor deficits [71]. This evidence concerns the gene TNFRSF1B and rheumatoid arthritis.