In the first instance, we not only confirmed our previous observation of increased expression of Fn14 in the skeletal muscle of SOD1G93A ALS mice during disease progression [33], but we also validated the previously reported negative correlation between the activity of the TWEAK/Fn14 pathway and the expression of the known molecular and metabolic effectors Glut4, Klf15, HKII and PGC-1α [29]. Here, PPARGC1A is linked to amyotrophic lateral sclerosis.