SPP1 and metabolic dysfunction-associated steatotic liver disease: In human MASLD, the association between ductular reaction and increased fibrosis is well recognized (49–51), while in rodent models of CLD, these biphenotypic ductular cells have been shown to promote myofibroblast activation, ECM deposition, and inflammatory cell infiltration (52–56) via secretion of key mediators such as PDGF (57), osteopontin (58), and chemokines (56, 59–61).