Our study has shown, for the first time to our knowledge, that ectopic overexpression of either miR-125b or miR-205, or silencing miR-424 expression, in the sensitive ER+ MCF-7aro cells was sufficient to trigger activation of the AKT/mTOR pathway, to develop de novo resistance to both letrozole and anastrozole drugs and to induce the selection of stem-like and tumor-initiating cells possessing self-renewing properties. The gene discussed is AKT1; the disease is neoplasm.