A primary pathogenic mechanism of gouty arthritis is that MSU crystals activate monocytes cells after being endocytosed, thus promoting the secretion of inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukins-1β (IL-1β), which will then cause an influx of inflammatory cells and strengthen the inflammatory reaction (Petrilli and Martinon 2007). The gene discussed is TNF; the disease is gout.