Moreover, p62 loss of function in zebrafish caused an abnormal locomotor phenotype; it was improved by an mTOR inhibitor (Rapamycin, an autophagy activator) and could also be rescued by wild-type human p62 expression but not by expression of the ALS-linked mutation p62P394L [110]. This evidence concerns the gene SQSTM1 and amyotrophic lateral sclerosis.