The potential higher efficacy of dose-dense FEC14 treatment in HER2 + patients than in HER2 − patients may be biologically explained by data suggesting that HER2 overexpression confers a high proliferative capability to the tumour (Borg et al, 1991) and is associated with an amplification of topoisomerase II alpha gene, a potential marker of anthracycline sensitivity (Di Leo et al, 2002). The gene discussed is ERBB2; the disease is neoplasm.