An anti-steatotic effect of Cl-IB-MECA in an HFD mouse model of NASH, induced by STZ administered 2 days after birth, was mediated via a molecular mechanism leading to decreased α-smooth muscle actin (αSMA, a marker of pathological fibroblasts) and cytokeratin 18 (CK-18, a predictor of NASH severity). Here, KRT18 is linked to metabolic dysfunction-associated steatohepatitis.