Taken together, these data indicate that the AO-1 inhibits TLR4/MyD88 signaling mediated pro-survival of paclitaxel in EOC cells and the combined use of AO-I with paclitaxel could improve tumor response to paclitaxel chemotherapy in patients with EOC by blocking MD-2-mediated activation of TLR4/MyD88 signaling. This evidence concerns the gene TLR4 and neoplasm.