Mechanistically, during liver fibrosis progression in NASH mice, hepatocytes redirect BAs from biliary secretion to systemic circulation by regulating the expression of BA synthesis enzymes (CYP7A1) and transporter (BSEP, NTCP and OSTβ), leading to increased systemic BA concentrations (Suga et al., 2019). This evidence concerns the gene SLC10A1 and metabolic dysfunction-associated steatohepatitis.