HER2 testing in breast cancer is currently performed either by immunohistochemistry for the HER2 protein or by fluorescence in situ hybridisation (FISH) analysis of the HER2 gene (Wolff et al., 2007).FISH can be performed with single-or dual-colour probes (Lambros et al., 2007).The use of the centromeric probe is recommended to correct the absolute HER2 copy number with the number of chromosomes 17, so as not to misinterpret chromosome 17 (Chrl7) polysomy as HER2 amplification.In fact, it has been reported that 8% of breast cancers show increased CEP 17 copy numbers by FISH (i.e.average CEP17 >3.0/nucleus) and these cases would represent Chrl 7 polysomy (Ma et al., 2005; Reddy et al., 2006; Wolffet al., 2007).On the other hand, it is well known that in HER2 amplified cancers Chrl 7 displays complex patterns of genetic aberrations, in particular involving its long arm (Arriola et al., 2008; Orsetti et al., 2004) and it has been suggested that some cases considered Chr17 polysomic may harbor amplification of the pericentromeric regions of CEP 17 (Isola et al., 2004).We performed an analysis of FISH defined Chrl 7 polysomic and disomic cases with microarray-based comparative genomic hybridisation and demonstrated that increases in CEP 17 copy number are only occasionally caused by Chr17 polysomy and can actually stem from high-level gains/amplification of CEP17 (Marchiò et al, submitted).These findings hold crucial implications for the selection of patients eligible for trastuzumab treatment.