Given that the liver expression of these three genes was up-regulated in the progression of MAFLD/MASH to hepatocellular carcinoma, and its inhibition delayed tumor growth and reduced the sphere-forming, proliferation, and clonality of liver cancer stem cells, it was proposed that the LPL/FABP4/CPT1 axis may regulate tumorigenesis by regulating fatty acid production, transport, and oxidation. Here, LPL is linked to liver cancer.