However, it is important to note that upon amplification of the ERBB2 gene, which occurs frequently in breast cancer (Slamon et al., 1987), the highly elevated levels of ErbB2 lead to violation of these physiological constraints and allow the formation of both ErbB2 homo-dimers and ligand-independent heterodimers (Worthylake et al., 1999; Yarden and Sliwkowski, 2001). This evidence concerns the gene ERBB2 and breast cancer.