Altogether, the results presented, especially the potent inhibition of MDA-MB-231 CDX and PDX TNBC tumor growth and metastasis in vivo, including robust in vivo targets engagement, and remarkable induction of apoptosis, with no apparent host toxicity, provides a strong scientific rationale for the development of racemic VNLG-152R as a novel therapeutic agent for TNBC, and possibly, other cancers and diseases driven by Mnk-eIF4E and mTORC1 signaling. This evidence concerns the gene ATP7A and neoplasm.