Arid1a loss drives non‐alcoholic steatohepatitis in mice via epigenetic dysregulation of hepatic lipogenesis and fatty acid oxidation. Arid1a loss drives non‐alcoholic steatohepatitis in mice via epigenetic dysregulation of hepatic lipogenesis and fatty acid oxidation

ARID1A, a DNA-binding component of the SWI/SNF ATP-dependent chromatin-remodeling complex, contributes to nucleosome repositioning and access by transcriptional regulators. Liver-specific deletion of Arid1a (Arid1a LKO) caused the development of age-dependent fatty liver disease in mice. Transcriptome analysis revealed upregulation of lipogenesis and down-regulation of fatty acid oxidation genes. Overall design: Livers of P90-day-old mice were collected, and transcriptomic analysis performed via RNA-seq.