It is worth mentioning that the various phenotypes associated with NASH that were observed in the context of Trim26 deficiency, such as increased liver weight, abnormal glucose metabolism, liver lipid accumulation, elevated levels of proinflammatory cytokines in the liver, altered expression profiles of genes related to inflammation, deposition of collagen fibres in the liver, and hepatocellular injury, were significantly mitigated when Cebpd expression was deficient (P < 0.0001 by one-way ANOVA; Fig. 5a–k and Supplementary Fig. 15d–f). Here, TRIM26 is linked to metabolic dysfunction-associated steatohepatitis.