PLAU and metabolic dysfunction-associated steatotic liver disease: Moreover, gene ontology (GO) analysis of canonical pathway showed that pathways involved in induction and progression of liver fibrosis (Urokinase-type plasminogen activator and its receptor; uPA-uPAR pathway [28]), FGF pathway [29], Integrin pathway [30], EphirinB pathway [31], liver cell apoptosis (potassium ion channel pathway [32]), nonalcoholic fatty liver disease (Natural killer T; NKT pathway [33]), acute and chronic liver disease (inflammation pathway [34]), were enriched in R778L-introduced HLCs compared to WT-HLCs (Figure S6).