Apart from the induction of chronic inflammation by ROS-mediated NF-κB activation, the active NF-κB is considered to be a key component in the rise of therapy-resistant cancers toward fractional gamma-irradiation therapy and chemotherapeutic agents such as 5-fluorouracil, bortezomib, cisplatin, daunorubicin, doxorubicin, paclitaxel, vinblastine, vincristine, and tamoxifen, through the transcriptional up-regulation of Akt, Bcl-2 (B-cell lymphoma 2), Bcl-xL (B-cell lymphoma- extra-large), cyclin D1, COX-2, survivin, and XIAP (X-linked inhibitor of apoptosis) [38,39,40,41,42,43]. The gene discussed is XIAP; the disease is cancer.