In conformity to that, we demonstrated an increased phosphorylation of JNK in the sciatic nerve of db/db mice which was reversed by CoPP, as occurs with this treatment in insulin resistant type 2 diabetic rats [37], as well as by SFN (a NRF2 activator) in db/db mice [20], revealing e that the antiallodynic effects triggered by the Nrf2/HO-1 signaling pathway in animals with type 2 diabetes were in part mediated via JNK inhibition. This evidence concerns the gene INS and type 2 diabetes mellitus.