Downregulation of phosphatase and tensin homolog (PTEN) in HCC [120] and simultaneous increased activation of the p85 subunit of phosphoinositide 3-kinase (PI3K) [119] through miR-21 conciliate to increase protein kinase B (AKT) signaling, thus limiting apoptosis signaling and promoting migration/invasion by indirectly inducing matrix metalloproteinases (MMPs). The gene discussed is AKT1; the disease is hepatocellular carcinoma.