Gouty arthritis (GA) is an acute inflammatory that is initiated by the precipitation of oversaturated solutions of uric acid as monosodium urate (MSU) crystals, which activates neutrophils to release neutrophil extracellular traps (NETs). NETs further enhance the inflammatory response by inducing neutrophils and monocytes to release pro-inflammatory cytokines and chemokines. However, the increasing number of neutrophils recruited to the sites of MSU deposits allows the formation of aggregated NETs that densely packs MSU crystals and degrades the proinflammatory cytokines, thereby allowing turning down the inflammatory. Here we briefly summarize the dual role of neutrophils during the initiation, development and the resolution of GA, and the signal pathways involved in the regulation of NETs formation.