Additionally, global knockout of galectin-3 (Lgals3), a member of the lectin family with a role in inflammation (Henderson and Sethi 2009), produces a fatty liver phenotype associated with PPAR-γ activation that progresses to fibrotic NASH and HCC (Nakanishi et al. 2008; Nomoto et al. 2006). This evidence concerns the gene LGALS3 and metabolic dysfunction-associated steatohepatitis.