More recently, using CRISPR-mediated MALAT1 activation or interference, the authors demonstrated that MALAT1 induces miR-125b degradation through the Ago2 complex, resulting in concurrent upregulation of miR-125b target genes BCL-2 and MMP13. Accordingly, silencing of BCL-2 and MMP13 neutralized the anti-apoptotic and invasion-promoting effect of miR-125b inhibitor on MALAT1 knockdown cells, thus confirming the role of these proteins in the establishment of cancer phenotypes in a MALAT1-overexpressing background. Here, MMP13 is linked to cancer.