PMP22 and Charcot-Marie-Tooth disease type 1A: Confirmation that overexpression of PMP22 is key to the pathogenic process driving CMT1A has been proven from clinical studies, demonstrating that children born to one parent with CMT1A and one with HNPP, carrying a duplication on one allele and no PMP22 gene on the other allele have no phenotype (PMID 19,513,300) [19].