Second, C75-induced FASN blockade was found to significantly prevent, to a similar extent, E2-stimulated AKT activity and E2-stimulated anchorage-independent growth of breast cancer cells, which has been shown to be mediated by non-genomic cross-talk between ERα and the PI3K/AKT pathway.45 Therefore, the interruption of AKT signaling might have a key role in determining the antiestrogenic actions that were observed following C75-induced blockade of FASN activity. The gene discussed is AKT1; the disease is breast carcinoma.