Despite evidence that β-catenin is a principal component of the canonical Wnt signaling pathway and that transcriptional response to Wnt signal activation is coordinated by a complex mesh of factors that bind to β-catenin in the nucleus [18], the mechanisms underlying MALAT1-mediated oncogenicity and CSCs-like phenotypes in HCC cells remain uncoupled with the activation of Wnt/β-catenin signaling. Here, MALAT1 is linked to hepatocellular carcinoma.