Through the genetic suppression of galectin-3, the authors demonstrated that galectin-3 levels in microglia contributed to HD pathogenesis in a nuclear factor-κB (NFκB)- and nucleotide-binding domain leucine-rich repeat and pyrin domain containing receptor 3 (NLRP-3) inflammasome-dependent manner. The gene discussed is LGALS3; the disease is Huntington disease.