In breast cancer models, high expression of TLR4 on tumor cells (166) leads to activation of the MyD88/NF-κB pathway upon recognition of HMGB1 in the tumor microenvironment, inducing the secretion of Matrix Metalloproteinase-9 (MMP-9) and Vascular Endothelial Growth Factor (VEGF), thereby enhancing tumor cell invasiveness and angiogenic potential (167). The gene discussed is NFKB1; the disease is neoplasm.