Actions and involvement of TNF-α as a primary mediator very much parallel those of IL-1β Levels of TNF-α are elevated in sciatic nerve after injury (82, 85) and Nadeau et al. (48) showed that microinjection of TNF-α into TNF-knock-out mice lowered mechanical pain threshold in a similar fashion to IL-1β TNF-α also upregulates Nav1.7 in DRG (89) and inhibition of TNF-α signaling results in attenuation or accelerated recovery from injury induced neuropathic pain (52, 84, 277). This evidence concerns the gene IL1B and neuropathic pain.