Thus, pharmacological inhibition of Mnk1/2, and, therefore, inhibition of both Mnk-eIF4E and mTORC1 pathways, might serve as a potential effective therapeutic approach for treating patients with advanced breast cancer including TNBCs and MBCs and possibly other malignancies with dysregulated Mnk-eIF4E/m-TORC1 signaling. Here, ATP7A is linked to maternal uniparental disomy of chromosome 20.