Similarly, Vitexin abolished the stemness of human hepatocellular carcinoma in vitro, as evidenced by the downregulation of the transcriptional activities of ATP-binding cassette subfamily G member 2 (ABCG2), acetaldehyde dehydrogenase 1 (ALDH1), and NANOG genes and by the overexpression of miRNA-34a; this latter event was also responsible for triggering apoptosis, as proven by the increase in Bcl-3 associated X protein (Bax)/B-cell lymphoma-2 (Bcl-2) and Bax/myeloid cell leukemia-1 (Mcl-1) ratios [79]. The gene discussed is BCL2; the disease is hepatocellular carcinoma.