CRS is mainly ascribed to a supraphysiologic release of a broad spectrum of pro-inflammatory cytokines, such as tumor necrosis factor alpha, (TNF-α), interleukin-2 (IL-2), and interferon-gamma (IFN-y), that can activate the monocyte/macrophage system, consequently triggering the production of a wide array of other pro-inflammatory proteins and result in increased C-reactive protein (CRP) levels and sometimes hyperferritinemia. The gene discussed is CRP; the disease is isolated hyperferritinemia.