Reverting back to the epithelial state by a mesenchymal-epithelial transition, making it difficult to isolate cells with true EMT markers. Studies in experimental mouse models have shown that a complete EMT-MET cascade is important for tumor metastasis. If the EMT process is so transient and, in parallel, so important for the development of metastatic tumors, why do only claudin-low and, to a lesser extent, metaplastic intrinsic molecular subtypes of BC present molecular features of EMT? One explanation could be that in claudin-low tumors the EMT-MET turnover is trapped in an intermediate mesenchymal state, in which EMT markers are present. We speculate that macroH2A1.1 stabilizes chromatin organizations characteristic of transcriptional programs linked to paused cell cycle progression. Hence, macroH2A1.1 expression could divert EMT-MET processes, stop progression and trap cells in such an intermediate state. High macroH2A1.1 mRNA ratios in the slow cycling claudinlow molecular subtype are correlated with earlier observations that macroH2A1.1 expression may be restricted to nonproliferative tissues, and that loss of its expression in lung and colon cancer was related to enhanced cell proliferation of cancer cells. In the 67NR mouse model which formed primary carcinomas when implanted into mouse mammary fat pads, Dardenne et al., identified a high macroH2A1.1/macroH2A1 ratio. Inversely, in the 4T1 mouse model, reduced macroH2A1.1 expression was correlated with macroscopic metastatic capacity in the lung. Our results point to high macroH2A1.1/ macroH2A1 ratios as markers of engaged but paused intermediate cellular stages of the EMT. Because the metastasic power of a tumor clearly depends on a complete EMT-MET process, it is tempting to propose a model in which macroH2A1.1 is linked to the EMT process and macroH2A1.2 linked to the MET process. TNBC is generally associated with a poor outcome, which is essentially not predicted by assessment of standard clinicopathological variables, such as lymph node status or tumour size at initial presentation. The lack of identified molecular targets in the majority of TNBCs implies that chemotherapy remains the treatment of choice for patients with TNBCs. Here we show that, regardless of the reason that led to an absence of adjuvant therapy for patients involved in the GSE31519 study, those with a high macroH2A1.1/macroH2A1 mRNA ratio have a worse prognosis than those with a low one. Even if this observation clearly needs to be confirmed with a larger cohort, it is tempting to propose that assessing macroH2A1.1 expression levels will allow the identification of TNBC patients who, despite favorable clinic-pathological variables such as lymph node status or tumour size at initial presentation, will have a worse prognosis and may benefit from treatment.