These authors also reported that, compared to untreated animals, mice treated with melatonin presented an increase in motoneuron loss and in the levels of 4-HNE, a marker of lipid peroxidation, as well as an upregulation of SOD1 expression, suggesting that melatonin exacerbates the disease phenotype in the SOD1G93A mouse ALS model (Table 2), by upregulating toxic SOD1, that overrides its antioxidant and antiapoptotic effects [199]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.