However, most of the currently available CMT2A models, which employ a neuron-specific promoter (HB9 or neuron-specific enolase) to drive expression of a mutant MFN2 transgene, elicit neuropathy only when the transgene is inherited from both parents (e.g.[28]), whereas CMT2A is almost always dominantly inherited; this discrepancy in inheritance pattern suggests that the pathogenesis of neuropathy in these mouse models may differ from the presumptively dominant negative mechanism responsible for the human disorder. This evidence concerns the gene MNX1 and neuropathy.