The activation of PTEN induced by MAF1 was observed to suppress Akt-mTOR signaling in liver cancer.35 Moreover, loss of tumor-suppressor PTEN and subsequent activation of PI3K/Akt pathway promoted human prostate cancer aggressiveness.36 Particularly, studies have shown that miR-10b regulated the self-renewal of the breast cancer stem cells phenotype by inhibiting PTEN and subsequently maintaining Akt pathway activation.37 As expected, our results showed that upregulation of PTEN in MCF-7 cells attenuated the promoting effect of overexpressed miR-106b and miR-93 on PI3K/Akt pathway. The gene discussed is MAF1; the disease is prostate carcinoma.