Rucaparib can inhibit NF-κB activation in response to DNA damage independent of SSB repair, increasing tumor cell sensitivity to irradiation. Rucaparib can also avoid the toxic effects associated with many classical NF-κB inhibitors without disrupting other key inflammatory activities. At a concentration of 1 μM, Rucaparid can reportedly inhibit 97.1% of PARP-1 activity in permeabilized D283Med cells. The gene discussed is PARP1; the disease is neoplasm.