Activated Toll-like receptors activate NF-κB via the cytoplasmic adaptor protein MyD88 and initiate transcription and expression of the precursor IL-1β gene, which is cleaved into mature IL-1β and secreted extracellularly, causing neutrophil recruitment and the release of more inflammatory mediators, producing an inflammatory cascade amplification reaction that induces acute gouty arthritis episodes [21–23]. The gene discussed is NFKB1; the disease is gout.