The mechanisms related to their therapeutic effects include inhibition of PI3K/Akt and PPTG1 signaling pathways, activation of LKB1-AMPK-P38MAPK-p53-survivin cascade resulting in cell death, and increased caspase-3-mediated vimentin hydrolysis leading to the death of breast cancer cells (164–167), indicating that it achieves the purpose of breast cancer treatment by regulating multiple signaling pathways. This evidence concerns the gene VIM and breast carcinoma.