Coincidentally, decreased dysregulated liver metabolism, lipid deposition, hepatosteatosis, and profibrosis, followed by reduced pro-inflammatory cytokines (e.g., IL-6, TNF-α, IL-1β, IL-18, and CCL2), and corresponding elevated anti-inflammatory factors (i.e., IL-10) were further observed by Trim26 overexpression in the WTDF-triggered NASH phenotype (P < 0.05 by 2 tailed t test; Supplementary Fig. S11b–k). Here, TRIM26 is linked to metabolic dysfunction-associated steatohepatitis.