In the hypoxic microenvironment of a steatotic-HCC mouse model, Jianxu et al. reported that upregulated HIF-2α expression led to lipid accumulation through PI3K-AKT-mTOR pathway activation, which reflected that the hypoxic conditions with HIF-2α upregulation could serve as a potential therapeutic target for liver cancer treatment [102]. The gene discussed is AKT1; the disease is liver cancer.