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. Here, LGALS3 is linked to amyotrophic lateral sclerosis.