In a streptozotocin (STZ) and high-fat diet (HFD)-induced hepatocarcinogenic mouse model, which mimics the nonalcoholic steatohepatitis (NASH)–hepatocarcinogenic process and closely follows human HCC progression32, conditional knockout of HK1 in HSCs of either Hk1f/f;Gfap-Cre mice or Hk1f/f;Lrat-Cre mice consistently retarded the development of HCC, accompanied by downregulated HK1 and Ki67 expression in primary tumor tissues (Fig. 4k–n). This evidence concerns the gene GFAP and metabolic dysfunction-associated steatohepatitis.