Thuringer et al. [78] explored that, in breast cancer cells, Hsp27—through the interaction with Toll-like receptor 3 (TLR3)—can activate NF-κB, which, afterward, leads to an increase in vascular endothelial growth factor (VEGF) expression and induces the secretion of VEGF-activating VEGF receptor type 2. This evidence concerns the gene NFKB1 and breast cancer.