However, this extracellular signaling can also establish a chemoresistant niche, as demonstrated in prostate cancer, where HMGB1 released from docetaxel-treated dying cells engages TLR4/RAGE on surviving tumor cells to activate NF-κB and induce secretory clusterin (sCLU), which in turn sequesters Bax and potently inhibits apoptosis [135]. Here, TLR4 is linked to neoplasm.