Conversely, it should be noted that in the study mentioned, overexpression of MFN2 specifically in neurons was found to rescue the loss of neuromuscular synapses and skeletal muscle atrophy in transgenic SOD1G93A mice (a mouse model of amyotrophic lateral sclerosis) and aged mice (a mouse model of skeletal muscle natural atrophy) [59]. Here, MFN2 is linked to Atrophy.