Furthermore, expression changes of genes related to (lipid) metabolism were noted in another wild-type FUS overexpression mouse model, as well as in a mutant FUS overexpression and FUS-ΔNLS-knock-in mouse model, suggesting a specific pathogenic mechanism contributing to FUS-mediated ALS [17, 50, 61]. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.