Considering that RIM1α is a protease substrate12 and that our previous publication demonstrated E3 ligase-dependent RIM1α ubiquitination crucially contributes to the development of neuropathic pain7, the possibility that RIM1α and Munc13-1 ubiquitination work synergistically to mediate spinal synaptic plasticity underlying neuropathic pain requires further investigation. This evidence concerns the gene UNC13A and neuropathic pain.