However, few studies have investigated the effect of VC on CSCs, the subpopulation responsible for tumor initiation, metastasis, recurrence, and resistance to chemotherapy.3,4 In this study, based on the elevated expression of SVCT-2, which is responsible for VC uptake, in liver CSCs, we revealed that clinically achievable concentrations of VC preferentially eradicated liver CSCs in vitro and in vivo. The gene discussed is SLC23A2; the disease is neoplasm.