Moreover, the use of high-throughput technologies has identified several molecular aberrations present in breast tumors including PIK3CA mutations, AKT, FGFR1, and CCDN1 amplifications, as well as PTEN loss that contribute to the activation of these pathways and therefore might propitiate endocrine resistance via non-classical activation of ER. This evidence concerns the gene AKT1 and breast neoplasm.