Epithelial–mesenchymal transition (EMT) in breast cancer is better understood as epithelial–mesenchymal plasticity (EMP), a dynamic and reversible spectrum of epithelial, hybrid, and mesenchymal states. In this review, we discuss how EMP is deployed differently across hormone receptor-positive/HER2-negative, HER2-positive, and triple-negative/claudin-low breast cancers, with distinct implications for metastasis, immune evasion, liquid biopsy, and therapeutic resistance. We highlight the regulatory networks and microenvironmental cues that shape state transitions and emphasize that hybrid and plasticity-high states may be more clinically informative than terminal mesenchymal states alone. We propose that progress will depend on subtype-aware, biomarker-guided strategies that resolve carcinoma cell state in space and time and therapeutically exploit EMT-associated vulnerabilities.