Inhibition of IL-6 at the moment represents a therapeutic target for the management of dysregulated host responses in patients with COVID-19 and is recommended in international guidelines in cases of severe disease [14]. A recent experimental model has shown that IL-6 increases FGF23 expression and contributes to the high levels of FGF23 in uremic mice completing a positive feedback loop in which IL-6 increases FGF23 expression that in turn may promote inflammation [15]. The gene discussed is FGF23; the disease is COVID-19.