Gout, the most common inflammatory arthritis, is the result of hyperuricemia and inflammation induced by monosodium urate (MSU) crystal deposition. However, most people with hyperuricemia will never develop gout, implying a molecular-genetic contribution to the development of gout. Recent genomic studies reveal links between certain genetic variations and gout. We highlight recent advances in our understanding of gout as an auto-inflammatory disease. We review the auto-inflammatory aspects of gout, including the inflammasome and thirteen gout-associated inflammatory-pathway genes and associated comorbidities. This information provides important insights into emerging immune-modulating targets in the management of gout, and future novel therapeutic targets in gout treatment. Cumulatively, this has important implications for treating gout as an auto-inflammatory disease, as opposed to a purely metabolic disease.
