A potential explanation for these findings is the previously recognized interaction between BRCA1 and elements of the histone deacetylation complex, including HDAC1 and 2 and the Retinoblastoma (Rb)-associated proteins RbAp46 and RbAp48.19 This interaction was mediated by the BRCT domain, which is truncated in the majority of BRCA1-mutated ovarian and breast tumors, including in the cellular models used in the current study, suggesting that the BRCT domain may be indirectly implicated in protein–protein interactions leading to chromatin remodeling and transcription regulation. This evidence concerns the gene RBBP7 and breast neoplasm.