This leads to the activation of molecules involved in AKT and MAPK signalling pathways that, in turn, phosphorylate and augment the functional activity of ER and the coactivator AIB1, rendering breast cancer cells resistant to endocrine therapy (Shou et al. 2004, Arpino et al. 2008) (Fig. 2). This evidence concerns the gene AKT1 and breast carcinoma.