The CAF-derived TGFβ then acts upon epithelial (carcinoma) cells and elicits the EMT; pharmacological inhibition of the secreted TGFβ, e.g., via a neutralizing antibody, has been shown to be effective at blocking the pro-EMT effects of breast cancer patient-derived CAFs on breast carcinoma cells [69]. This evidence concerns the gene TGFB1 and breast carcinoma.