Genetic ablation of PPARα or inhibition of FAO by the CPT1 inhibitor etomoxir significantly blocked the development of β-catenin-activated HCC in mice, suggesting that β-catenin controls the dependence on FAO for HCC development, and that FAO is the driving force for β-catenin-activated HCC (Figure 2B). The gene discussed is CPT2; the disease is hepatocellular carcinoma.