We propose that when overlapping each molecular BC subtype across the continuum of cHER2+, where one extreme is the complete absence of CD44+CD24−/low M-CSCs in HER2-enriched/cHER2+ tumors and the other extreme is a high preponderance of CD44+CD24−/low M-CSCs in basal/cHER2+ and claudin-low/cHER2+ tumors, the differential enrichment of ALDH-expressing versus CD44+CD24−/low CSCs might explain both the clinical behavior and the primary efficacy of trastuzumab in each mixed cHER2+ subtype (Figure 2). This evidence concerns the gene CD44 and breast cancer.