Similarly, overexpression of miR-216a/217 induced EMT through activation of PI3K (phosphatidylinositol 3-kinase)/Akt and TGF-β (transforming growth factor, beta 1) pathways by targeting PTEN (phosphatase and tensin homolog deleted on chromosome ten) and SMAD7 (SMAD family member 7), leading to contribution to tumor recurrence in HCC [13]. This evidence concerns the gene SMAD7 and neoplasm.