Indeed, an equivalent overlapping of the intrinsic BC subtypes across the continuum of cHER2-negative BC can explain the apparently paradoxical activity of trastuzumab in HER2e/cHER2− and luminal/HER2− tumors [66, 67], which accumulate HER2-dependent (but not due to gene amplification) ALDH-overexpressing E-CSCs. The gene discussed is ERBB2; the disease is breast cancer.