Hyperactivation of BCL2 interacting protein3 (BNIP3) reprograms glycolysis to increase lenvatinib resistance (LR) in HCC.5 From a detailed analysis of heterogeneity of HCC by patient-derived tumor xenograft organoids (PDOs), a key molecule c-Jun was identified to promote stemness of HCC and LR through the β-catenin pathway. This evidence concerns the gene JUN and hepatocellular carcinoma.