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This manuscript presents a mechanistic hypothesis for the durable, non-chemotherapeutic control of breast cancer metastasis by combining two complementary strategies: (1) metabolic niche normalization through inhibition of the monocarboxylate transporters MCT1 and MCT4, and (2) pharmacological reactivation of the NR2F1 dormancy program. The central hypothesis is that metastatic outgrowth is governed by a metabolic–epigenetic switch, and that simultaneous normalization of the acidic, lactate-rich tumor microenvironment together with reinstatement of NR2F1-mediated dormancy will stabilize disseminated tumor cells in a long-term quiescent state, thereby reducing metastatic recurrence.

This work does not present new experimental or clinical data. Instead, it integrates published evidence into a unified conceptual framework and proposes a series of falsifiable predictions and experimental approaches designed to test the hypothesis in breast cancer cell lines, organoids, and animal models. The manuscript is intended to stimulate scientific discussion, encourage experimental validation, and foster collaboration in the fields of cancer dormancy, metastasis, and cancer metabolism.