Additionally, Pparα, phosphatase and tensin homolog (Pten), cyclin-dependent kinase inhibitor 1A (Cdkn1a), spectrin beta, non-erythrocytic 1 (Sptbn1), and mediator complex subunit 1 (Med1), all of which are involved in biological pathways responsible for the development of NAFLD, exhibited altered H3K9me3 and H3K4me3 status in lipid-loaded hepatocytes. This evidence concerns the gene CDKN1A and metabolic dysfunction-associated steatotic liver disease.