During EMT, cancer cells lose their epithelial properties and develop a more mesenchymal, migratory phenotype, which boosts their ability to invade neighboring tissues and spread to distant regions.315,316 This process is mediated through various signaling pathways, primarily the canonical TGF-β/SMAD pathway, which activates transcription factors that promote the EMT program.316 For example, a recent study reported that TGF-β-dependent signaling plays a central role in promoting EMT during advanced stages of BC. This evidence concerns the gene TGFB1 and breast cancer.