Tumours from bitransgenic animals overexpress ErbB2, making them candidates for ErbB2-targeted therapy, but drugs which molecularly target ErbB2 (such as trastuzumab) or ErbB2/ErbB3 heterodimers (such as pertuzumab) may be futile because signalling downstream of ErbB2/ErbB3 is already attenuated in bitransgenic animals. Here, ERBB2 is linked to neoplasm.