This was based on the observation that ATF3 was predicted to be highly functionally related to NFκB during regulation of cell cycle and cytokine metabolic process (Table 1) and to indirectly bind to NFκB via NR4A2 after phosphorylation by MAP3K8 (Fig 2); notably, previous findings only observed ATF3 as a co-repressor with NFκB in prostate cancer [53]. The gene discussed is ATF3; the disease is prostate carcinoma.