Given that p120‐Catenin stabilizes E‐Cadherin at the membrane (Jin et al. 2024; Kourtidis et al. 2013), the increased distribution of p120‐Catenin at SLIs may represent a compensatory response to adherens junction disruption, potentially resulting in better preservation of junctional integrity in HNPP than CMT1A. The gene discussed is PMP22; the disease is hereditary neuropathy with liability to pressure palsies.