In summary, our evaluation of the association between Aurora A and Bcl-xL copy numbers and expression and epithelial/mesenchymal phenotypes in TNBC shows that the co-expression of Aurora A and Bcl-xL is associated with the invasion capability of TNBC cells in the basal B subtype, and inhibition of both molecules is required to suppress tumor metastasis. The gene discussed is BCL2L1; the disease is neoplasm.