However, we note that CRMP2 K374A knock-in mice, in which the SUMOylation site on CRMP2 at Lys 374 was replaced by an alanine, did not exhibit any sexual dimorphism in multiple parameters, including in long-term potentiation, compulsive- or depression-associated behaviors, response to thermal stimulation, excitatory neurotransmission in the spinal cord, licking responses to injection of the pan sodium-channel activator veratridine, and in their refractoriness to developing persistent mechanical allodynia fin the spared injury model of neuropathic pain [25]. This evidence concerns the gene DPYSL2 and major depressive disorder.