The authors observed that deletion of Phd1-3, which increased HIF2α stabilisation still further, did worsen steatosis, suggesting that lower level HIF2α activation may be predominantly beneficial via improved insulin sensitivity, while higher levels of stabilisation, as occurs with Phd1-3 and Vhl deletion (and potentially in long-term NAFLD) has a detrimental effect due to inhibition of FAO, leading to worsened steatosis. The gene discussed is VHL; the disease is steatosis.