Since resistance to anti-HER2 therapies may be caused by downmodulation of HER2 expression ([10], see also Figs 3 and 4), it was reasonable to hypothesize that amplification of HER2 in DM would endow breast cancers with the ability to modulate HER2 protein expression and, thus, sensitivity to anti-HER2 therapies by dynamically regulating HER2 copy number. Here, ERBB2 is linked to breast carcinoma.