This is evidenced by deregulated levels of Ankrd1, Fbxo32, Nogo A and Rrad causing induction of muscle differentiation and a subsequent increase in expression levels of Myog, Myod1, Myf5, Pax7 and Mef2c (although this is not significant for Mef2c) or overexpression of Mt2, Sln and Impa1 in response to increasing oxidative stress levels and alterations in calcium and glucose homeostasis, previously described as characteristics of ALS [22]. This evidence concerns the gene SLN and amyotrophic lateral sclerosis.