In glial cells, ADAM17 facilitates the proteolytic cleavage of proinflammatory cytokines such as TNF-α, IL1-β, and IL6-R, increasing chronic inflammation and neuronal dysfunction in diabetic neuropathy and CNS injury [63,64], or conversely, genetic knockdown of ADAM17 in glial cells suppresses neuroinflammatory cytokine release and reduces glial overactivation [65,66]. This evidence concerns the gene IL1B and diabetic neuropathy.