Since human tumours exclusively overexpress the wild-type ErbB2 rather than the transforming point mutant (Lemoine et al, 1990), a reasonable hypothesis is that tumour cells acquire a growth advantage from wild-type ErbB2 overexpression, but that this phenotype does not represent the primary transforming event – implying the co-existence, that is, of at least one other molecular defect within the tumour cells. Here, ERBB2 is linked to neoplasm.