In contrast, the AF-resistant mesenchymal-like TNBC cell lines have enriched expression of genes associated with the epithelial-to-mesenchymal transition (e.g., TGFβ, mTOR, ALK, Wnt/β-catenin) and cell motility (Rac1/Rho, focal adhesion, integrin signaling) pathways [12], suggesting that drugs targeting these aberrant pathways could be used to treat mesenchymal-like TNBC. This evidence concerns the gene ALK and atrial fibrillation.