We therefore submit that human tissues with cell-cycle control defects (De Cremoux et al, 1999; Prevo et al, 1999) may gain a growth advantage by prolonging and intensifying ambient growth factor signals via ErbB2 upregulation, and that tumour cells overexpressing ErbB2 may in turn clonally select for cell-cycle checkpoint loss (Li et al, 1997). Here, ERBB2 is linked to neoplasm.