The cases with dHMN due to the splice-site mutation c.151+1G>T, resulting in deletion of the last 20 amino acids encoded by exon 1, had a later age at onset and lacked spasticity.8 As suggested by the authors, this phenotype is similar to that described in patients with dHMN and pyramidal features identified in the Jerash region of Jordan (dHMN-J) and mapped to 9p21.1-p12, which encompasses SIGMAR1. This evidence concerns the gene SIGMAR1 and distal hereditary motor neuropathy.