In line with these studies, the heightened ERK activity, as well as the overproduction of TNFα and IL-1β in the DRG of lupus mice with chronic pain, further support the notion that neuroinflammation at the DRG may contribute to the genesis of hyperexcitability in the nociceptive sensory neurons and chronic pain in lupus mice. This evidence concerns the gene TNF and systemic lupus erythematosus.