Although the presence of Rb may be required for BRCA1-mediated growth arrest, the interaction of these two proteins might not. Indeed, Rb acts as a downstream effector of several growth suppression pathways.
The complex containing Rb and histone deacetylase is thought to suppress transcription of E2F-responsive genes. Given the proposed role of BRCA1 in transcriptional regulation, one possible explanation for Rb-dependent BRCA1 growth suppression is that BRCA1 targets the Rb-histone deactylase complex to specific genes regulated by progression through the cell cycle.
If Rb is a modulator of BRCA1 action, it is conceivable that reduction in the level of Rb expression in breast epithelia may induce a BRCA1 'null' phenocopy in BRCA1 carriers with potentially reduced BRCA1 expression. If this were the case, factors augmenting Rb expression might serve to delay the onset of cancers in these susceptible women.