The pathophysiology of MAS involves dysregulated macrophage and cytotoxic T-cell activation, resulting in a “cytokine storm” driven by interleukin (IL)-1β, IL-6, tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ), which contribute to severe systemic inflammation, persistent fever, cytopenias, hyperferritinemia, and multiorgan dysfunction [1,4,5]. The gene discussed is IL6; the disease is isolated hyperferritinemia.