Pathogenesis of gout inflammation remains unknown, but recent advances have been made with respect to initiation, amplification, and self-limitation. Direct crystal-cell membrane contact leads to cell activation, involving membrane-associated molecules. Resolution of acute gout inflammation is a mechanism that is controlled by monocyte-macrophage switch, which results in the loss of cytokine production capability and, conversely, the ability to produce anti-inflammatory molecules. MRI and ultrasound findings provide preliminary data that are not yet used in clinical trials. Diagnosis and management recommendations are missing, but this gap will be filled soon with the upcoming European League Against Rheumatism Task Force's recommendations on gout.