Notably, the occupancy of H3K14ac at the SREBF1 promoter remains unchanged, with H3K14ac partially colocalizing with H3K9me3 and SETDB1, indicating a poised inactive state to alter SREBF1expression, ultimately inhibiting the SREBF1-FASN/SCD1 axis mediated lipid metabolism and thereby blocking HCC progression (Fig. 7). This evidence concerns the gene SETDB1 and hepatocellular carcinoma.