Charcot-Marie-Tooth (CMT) disease, a hereditary motor and sensory neuropathy, is the most common inherited disorder of the peripheral nervous system with a prevalence of 1/2500 [1]. It is a genetically and clinically heterogeneous group of disorders with the most common type designated as CMT1 [2]. The majority of CMT1 cases are due to reciprocal 1.5 Mb duplication/deletion in chromosome 17p11.2, that results in two clinically different neuropathies named CMT1A and HNPP, respectively [3]. CMT1A is demonstrated by progressive symmetrical weakness and atrophy of the distal limb muscles, reduced or absent deep-tendon reflexes, decreased nerve conduction velocities and characteristic segmental de- and remyelination named “onion bulb formation” [4]. HNPP is characterized by recurrent nerve palsies resulting from minor trauma. Histopathological findings from nerve biopsies of HNPP patients show typical sausage-like thickening called “tomacula” [4]. Both CMT1A and HNPP are responsible for about 80% of autosomal-dominant CMT1 cases. The duplicated/deleted region encompasses the genes responsible for expression of peripheral myelin protein 22 (PMP22) and a gene dosage