During the course of analysis of the role of estrogen in activating EMT, we observed that E2 stimulated expression of p-Akt, p-Gsk3β, and p-4Ebp1, downstream targets of Akt, in p18−/−;Brca1MGKO tumor cells, which was not blocked by 4OHT (Fig. 3e, g). The gene discussed is AKT1; the disease is neoplasm.