The recent mouse model expressing a BRCT mutant of BRCA1 (S1598F, corresponding to human BRCA1 S1655F) incapable of binding to phospho-peptides in place of the wild type allele of BRCA1 failed to suppress breast tumor development further confirms that the BRCT domain and its capability to bind phosphorylated protein is required for the tumor suppressor function of BRCA1 [21]. This evidence concerns the gene BRCA1 and neoplasm.