In 1997, Oh et al. (Oh et al., 1997) hypothesized that the primary defect underlying CMT1X neuropathy in the presence of Cx32 mutants forming electrically conductive channels is the lower permeability of GJ channels to cAMP, which is involved in myelin homeostasis in SCs (LeBlanc et al., 1992). The gene discussed is GJB1; the disease is neuropathy.