This result seems controversial with the well-established concept that MiR-205 expression inhibits, rather than promotes, EMT program by targeting ZEB1/2, leading to an increased E-cadherin in breast, bladder and prostate cancers.14, 43, 44 Nevertheless, despite detailed mechanisms remain unknown, Li et al.45 reported that MiR-205 expression is associated with the E-cadherin suppression during the development of extra embryonic endoderm, which is in consistent with our results. The gene discussed is CDH1; the disease is prostate cancer.