Evidence of the roles of MSK1 and MSK2 in the development and persistence of pain is emerging; global depletion of both MSK isoforms specifically inhibits the development of inflammatory heat hyperalgesia, while MSK1 contributes to the sustained component of pain evoked by activation of chemosensitive primary sensory neurons by formalin and developing after peripheral sensory neuropathy [11,12,13,14]. Here, RPS6KA5 is linked to sensory peripheral neuropathy.