In TNBC cell lines, paclitaxel treatment was found to increase IRAK1 phosphorylation, leading to acquired resistance and cancer stem cell enrichment; sensitivity to low doses of paclitaxel was restored by co-administration of IRAK1/4 inhibitor I, with the combination inducing massive apoptosis involving both NF-κB and p38-MCL-1 signaling pathways. Here, NFKB1 is linked to cancer.