As the majority of Cx32 mutations implicated in CMTX1 are loss-of-function [12, 13], the hypothesis is that reduced permeability of mutant GJCs to signaling molecules, such as cyclic adenosine monophosphate (cAMP), disrupts myelin homeostasis and contributes to CMT1X neuropathy [14, 15]. This evidence concerns the gene GJB1 and neuropathy.