Increased expression of Gal-3 in HD mice induced inflammation through nuclear factor kappa-B (NF-κB) and nucleotide-binding oligomerization domain-like receptor (NOD), leucine-rich repeat- (LRR), and pyrin domain-containing protein 3 (NLRP3) inflammasome-dependent pathways, while the silencing of Gal-3 suppressed inflammation, improved motor dysfunction, and increased survival in HD mice (Siew et al., 2019). Here, LGALS3 is linked to Huntington disease.