Chronic inflammation is known to be a key player in the pathophysiology of CLL, as evidenced by the increased production of inflammatory cytokines (such as IL-6, IL-10, IL-8, TNF-α, and IFN-γ) and chemokines, alongside the activation of intracellular pro-inflammatory signaling pathways [46,47,48]. The gene discussed is TNF; the disease is B-cell chronic lymphocytic leukemia.