Additionally, functional loss of hepatocyte Trim26 accelerates HFHC/WTDF-triggered NASH-associated fibrosis pathologies, as evidenced by increased liver α-Sma contents, serum TGF-β, hepatic hydroxyproline levels, corresponding pro-fibrotic factors, e.g., α-Sma, Tgfb, Ctgf, Col1a1, Col3a1 mRNA abundance, and pro-fibrotic factors levels in the HKO HFHC/WTDF-Serum-treated primary HSCs assay (P < 0.05 by 2 tailed t test; Supplementary Fig. 8a–h). The gene discussed is TRIM26; the disease is metabolic dysfunction-associated steatohepatitis.