In particular, there are clear examples of how NF-κB activation mediates acquired drug resistance, as seen in a recent study that demonstrated upregulation of NF-κB signaling as a key mechanism underlying acquired resistance to poly-adenosine ribose polymerase (PARP) inhibition, a class of anti-cancer drugs with proven activity in BRCA mutant cancers, while showing significant results that co-treating cancer treatment with an NF-κB inhibitor may reverse the acquired resistance [84]. This evidence concerns the gene PARP1 and cancer.