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Charcot-Marie-Tooth (CMT) neuropathy remains one of the most common and genetically diverse neuromuscular disorders within the neurologic field. Mutations in >120 genes reflect the genetic heterogeneity of CMT, the most common form being attributable to a PMP22 gene duplication (type 1a; CMT1A). CMT is broadly classified by inheritance type (dominant, recessive, or X-linked) and electrophysiology (demyelinating with upper limb motor conduction velocities <38 m/s, axonal with velocities ≥38 m/s, or intermediate with conductions >35–45 m/s).1 A distal pattern of generally slowly progressive motor and sensory deficits referable to the peripheral nervous system defines its clinical phenotype, although forms with purely sensory, purely motor, or mixed sensory and autonomic features also fall under the umbrella of the disorder. Characteristic foot deformity and family history are important clues guiding the clinician to the diagnosis.