In hereditary demyelinating neuropathies conduction slowing has been reported to be uniform between and within nerves. This practical criterion has been used in the differential diagnosis with acquired demyelinating disorders. We report a 55‐year‐old man complaining of weakness and paresthesias of right hand and weakness of right leg. Examination showed bilateral pes cavus, difficulty to walk on heels, mild distal weakness in upper limbs, more on the right, and reduced reflexes in lower limbs. CSF was normal. Electrophysiological study showed a demyelinating sensory‐motor polyneuropathy with non‐uniform slowing of motor conduction, abnormal amplitude reduction with temporal dispersion of proximal motor responses in median and ulnar nerves. Sural biopsy was consistent with a demyelinating neuropathy. Chronic inflammatory demyelinating polyneuropathy (CIDP) was diagnosed and the patient treated with prednisone with improvement of paresthesias. Four years later the patient's brother, 57 years old, was referred for cramps, fasciculations and paresthesias in extremities. Examination showed mild distal weakness and atrophy, pes cavus, and reduced or absent reflexes. CSF examination showed slightly increased proteins and conduction slowing was uniform. Molecular analysis revealed in both patients an Arg(15)Gln Cx32 mutation.Non‐uniform conduction slowing has been recently re‐ ported in a CMTX family with Arg(15)Trp mutation (same codon of our patients) and in a woman with a non sense mutation at codon 102. The possibility of a CIDP‐like electrophysiological pattern in some CMTX patients should be kept in mind to avoid misdiagnoses.