In our study, highly migratory MRC5 lung fibroblasts and MDA-MB-231 breast cancer cells (wildtype PI3K and BRCA1, mutated KRas (G13D) [28] and mutated P53 (missense mutation) [29]) were both used to probe the response of dual-inhibition of the eIF4E-MNK pathway and PI3K-AKT-mTOR pathways (Figure 1). This evidence concerns the gene ATP7A and breast carcinoma.