A recent study proposed miR34a as a viable biomarker in the follow-up of ES disease, even though miR-185 was shown to be involved in ES cell proliferation, motility, and survival by downregulating the PI3K/Akt/mTOR and Wnt/β-catenin pathways, which functions as a tumour suppressor. This evidence concerns the gene AKT1 and neoplasm.