This regulatory mechanism has been experimentally validated in hepatocellular carcinoma (HCC) by Shi et al. The genetic knockdown of UBE2O significantly enhances AMPKα2 protein stability, whereas its overexpression reduces AMPKα2 levels and enhances mTOR phosphorylation (p-mTOR), thereby promoting the transcriptional activation of downstream target genes (including MYC, Cyclin D1, HIF1α, and sterol regulatory element-binding protein 1/SREBP1) [28]. Here, HIF1A is linked to hepatocellular carcinoma.