Thus, when contemplating a continuum of epithelial-like and mesenchymal-like CSC states throughout the overlapping molecular BC subtypes in cHER2+, it becomes obvious that the EMT phenomenon is a pivotal mechanism that, when activated, convergently drives primary and secondary resistance to HER2-targeted therapies (for a more detailed explanation of how the EMT phenomenon impacts intra-tumor heterogeneity and trastuzumab efficacy in cHER2+ BC, see BOX1). Here, ERBB2 is linked to breast cancer.