VP treatment led to YAP, AXL, CYR61 and/or CTGF downregulation in the BC cell lines of different subtypes, suggesting that these effectors may act as their own target genes as described in TNBC MDA-MB-231 cells, VP could inhibit the transcriptional activity of TEAD, reduce the protein expression levels of YAP target genes, AXL and CTGF, inhibit the migration, and induce the apoptosis of paclitaxel resistant MDA-MB-231 cells [27–29]. The gene discussed is CCN2; the disease is breast cancer.