Autoantibodies such as antinuclear antibodies are generally not detected, however, it is thought that hypercytokinemia involving interleukin-1β (IL-1β), IL-6, IL-18, and tumor necrosis factor-α, due to abnormal activation of innate immune cells such as monocytes and macrophages, may be involved in disease pathogenesis.[12] The clinical course of AOSD is divided into 3 types: monophasic, intermittent, and chronic.[13–15] Long-term treatment is particularly essential in intermittent and chronic types in which systemic symptoms relapse repeatedly. The gene discussed is IL6; the disease is adult-onset Still disease.