Prevailing views indicate that stimulation of these receptors by adenosine triphosphate (ATP) turns on the p38 mitogen-activated protein (MAP) kinase and nuclear factor κB (NF-κB) pathways in microglia, triggering synthesis and release of a variety of proinflammatory agents including interleukin-6 (IL-6), tumor necrosis factor–α (TNFα), and IL-1β, which potentiate excitatory synaptic transmission in the dorsal spinal horn and remodel spinal circuits involved in neuropathic pain (3, 4, 8). Here, IL6 is linked to neuropathic pain.