Twenty percent of MFN2 mutations are de novo. Occasional CMT2A patients also have optic atrophy (these cases were termed HMSN VI in previous classifications)[25] brisk reflexes, and / or minor white matter changes on brain MRI.[26] Mutations in MPZ and NEFL can also cause the classical AD CMT2 phenotype as mentioned above. This evidence concerns the gene MFN2 and Leber hereditary optic neuropathy.