Exploiting our understanding of the critical role of aberrantly expressed MALAT1 and activated Wnt/β-catenin signaling in the oncogenicity and stemness activities of several solid tumor types [6,7,8,9,10,11], the present study summarily provides evidence that aggressive HCC cells are characteristically MALAT1high and that this positively correlated with an enhanced CD133highCD90high HCC-SCs pool and associated with Wnt/β-catenin signaling-mediated marked up-regulation in HCC oncogenicity and pluripotency. The gene discussed is MALAT1; the disease is hepatocellular carcinoma.