Type 2A CMT (CMT2A) is caused by mutations of the mitochondrial fusion protein, mitofusin 2 (MFN2) (Züchner et al., 2004), and is distinguished from other CMT subtypes by onset of neuromuscular signs in early childhood and progressive loss of neuromuscular coordination and strength in arms throughout the first two decades of life, thought to be the consequence of dying-back of long peripheral nerves (Fridman et al., 2015; Feely et al., 2011; Bombelli et al., 2014; Yaron and Schuldiner, 2016; Berciano et al., 2017). This evidence concerns the gene MFN2 and Charcot-Marie-Tooth disease.