In prostate cancer, inflammatory cues activate I kappa B kinase beta (IKKβ) to phosphorylate ARID1A, leading to its degradation via E3 ubiquitin ligase β-TRCP; ARID1A downregulation, in turn, silences the enhancer of A20 deubiquitinase, a critical negative regulator of NFκB signaling, and thereby unleashes C-X-C motif chemokine receptor 2 (CXCR2) ligand-mediated myeloid-derived suppressor cell chemotaxis that permits cancer progression [33]. The gene discussed is ARID1A; the disease is Familial prostate cancer.