Treatment with PMP22-targeting ASO or microRNA ameliorated the deficits in CMT1A mouse models, including declines in NCV and CMAP, demyelination in peripheral nerves, and motor disabilities (19, 20); however, an excessive reduction in PMP22 is associated with a risk of HNPP-like symptoms. The gene discussed is PMP22; the disease is hereditary neuropathy with liability to pressure palsies.