TNF and amyotrophic lateral sclerosis: Deletion of Gal-3 in a mouse model of ALS resulted in rapid disease progression, and increasing in microglia, TNF-α, and oxidative injury (Lerman et al., 2012), suggesting that endogenous production of Gal-3 by microglia may, at least in part, limit neuroinflammation and disease progression during ALS.