TNF and metabolic dysfunction-associated steatohepatitis: Moreover, Chromatin Immunoprecipitation Sequencing (ChIP-Seq) using liver tissues from patients with non-alcoholic steatohepatitis (NASH) revealed that H3K27ac enrichment increases at gene loci associated with tumor necrosis factor α (TNFα) signaling inflammatory responses, epithelial-to mesenchymal transition, and IL2-STAT5, while BRD4 inhibition significantly reduced NASH-induced hepatocarcinogenesis [111].