Second, somatic inactivation of the wild-type BRCA1 allele may not be the only mechanism of breast cancer development in BRCA1 mutation carriers, as at least a subset of BRCA1-driven tumors appear to retain BRCA1 function [64, 65]; it is tempting to speculate that the sensitivity to taxanes is preserved in the latter category of BC. This evidence concerns the gene BRCA1 and breast cancer.