Hepatocytes cultured with free fatty acids overexpress the ATP-dependent chromatin remodeling proteins Brg1 and Brm, which upon recruitment to proinflammatory genes stabilize nuclear factor kappa B (NF-κB) binding and help remodel chromatin.51 Impressively, experimental depletion of Brg1 into MCD-fed mice suppressed steatosis, inflammation, and fibrosis, indicating a pivotal role for Brg/Brm chromatin remodeling proteins in the progression of NAFLD. Here, SMARCA2 is linked to metabolic dysfunction-associated steatotic liver disease.