This modification subsequently activates the NF-κB signaling cascade, leading to increased expression of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 alpha (IL-1α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), thereby facilitating tumor progression (53). The gene discussed is TNF; the disease is neoplasm.