Truncated mutations of APOB are speculated to result in decreased very low-density lipoprotein synthesis, diverting energy into cancer-related metabolic pathways.27,28 Activation of CTNNB1 is thought to rewire fatty acid catabolism, resulting in reduced lipogenesis and increased use of fatty acids as an energy source.29,30 Silencing of CPS1 in HCC is linked to an in increased CAD expression, leading to increased pyrimidine synthesis, allowing for increased cell proliferation.6 This evidence concerns the gene CTNNB1 and cancer.