Although it has been proposed that FAK was critical for migratory behaviour whereas Pyk2 was involved in the proliferative phase of ErbB2 tumour induction in vitro [8], the observation that FAK-null ErbB2 tumours can form metastatic lesions argues that at least in the in vivo setting, Pyk2 can functionally substitute for FAK. The gene discussed is ERBB2; the disease is neoplasm.