After 48 h of rapamycin (autophagy activator) and 3-methyladenine (autophagy inhibitor) treatments, the exogenous activation of the mTOR-autophagy pathway, but not inhibition of the pathway, in ALS astrocytes significantly reduced the concentrations of TNFα, IL1β, and IL6 in cell culture medium and reduced the levels of p62, while increasing the levels of LC3B-II/LC3B-I, ULK1, and p-Beclin-1 (Ser15), and these changes were comparable to those in control subject astrocytes. This evidence concerns the gene BECN1 and amyotrophic lateral sclerosis.