The study of diabetic neuropathy in rats has shown that the deficit in IR signaling is associated with exacerbated hyperalgesia (3) or that intrathecal insulin delivery can accelerate axon regeneration and rescue the retrograde loss of collateral axons after peripheral nerve injury (36, 37) Compared to pre-CCI levels, insulin receptor-1 (IR-1) expression increased in male and female mice following experimental neuropathy. The gene discussed is INS; the disease is diabetic neuropathy.