Since elevated level of phospho-NEFL was reduced by inhibitor or by the Cdk5-specific shRNA and the reduced mitochondrial movement, which is mediated by reduced acetylated-α-tubulin, was recovered by the utilization of HDAC inhibitor [18], targeting Cdk5 or HDAC could be the therapeutic strategies for the treatment of axonal neuropathy caused by the mutation in HSP27. The gene discussed is HSPB1; the disease is axonal neuropathy.