Furthermore, in SOD1G93A and Smn2B/- mutant mice, which mimic the human MN diseases ALS and SMA, respectively, degenerating MNs exhibit increased nuclear Y172 immunoreactivity, indicative of c-Jun activation in injured MNs, but a marked depletion in C-bouton-associated Y172-positive profiles, which is consistent with the loss of afferent inputs that occurs in MN diseases (Ling et al., 2010; Mentis et al., 2011; Moreno-López et al., 2011; Sunico et al., 2011; Tarabal et al., 2014; Milan et al., 2015; Cerveró et al., 2018). This evidence concerns the gene JUN and amyotrophic lateral sclerosis.