Given the important role of NF-κB and its dependency on IRAK1 in TNBC progression, we reasoned that therapeutic targeting of IRAK1 might be able to achieve cancer selectivity, thus being a more accessible and less deleterious target than NF-κB itself for curtailing TNBC or other high IRAK1- and NF-κB-driven cancers. Here, NFKB1 is linked to cancer.