Thus, BRCA1 wild type cancers are more sensitive to taxanes due to BRCA1 mediated inhibition of MT nucleation and centrosome regulation as compared to BRCA1 mutant cells that have reduced γ-tubulin monoubiquitination, elevated rates of MT polymerization/depolymerization, and centrosome amplification that potentially hinder taxanes from binding to MTs [19, 24, 25, 28–30]. This evidence concerns the gene BRCA1 and cancer.