Finally, our study emphasizes the importance of driver genetic alterations found in minor subgroups of breast cancer, given that SF3B1 mutant cells were shown to be selectively sensitive to a potent SF3b complex inhibitor, spliceostatin A, suggesting that inhibition of the spliceosome complex may constitute a novel therapeutic strategy for patients with SF3B1 mutations independent of tumour type. This evidence concerns the gene SF3B1 and breast cancer.