PMP22 and Charcot-Marie-Tooth disease type 1E: With this background in mind, several non-exclusive pathomechanisms have been proposed for CMT1A with some variations of these considered for HNPP and CMT1E including altered myelin architecture and function due to abnormal PMP22 membrane stoichiometry, PMP22 protein aggregation/ER stress, disrupted axonal architecture and transport, Schwann cell death, and secondary axon degeneration due to myelin dysfunction [37,41].