MFN2 and Charcot-Marie-Tooth disease type 2A1: Interestingly, a TAT-peptide-mediated strategy has been demonstrated to be effective in destabilizing the tethering-non-permissive HR1−HR2 interaction, correcting the fusion defects observed with some MFN2 mutants linked to Charcot−Marie−Tooth disease type 2A (CMT2A, see below)27.