The proposal that thrombus formation could stimulate inflammation through hypoxia and HIF activation is also consistent with the observation that organ dysfunction in sepsis may be reversible [5], given that thrombus resolution is stimulated by hypoxia and activation of HIF1 and followed by temporal reductions in the severity of hypoxia and in the expression levels of HIF1α [15, 16, 33, 34]. The gene discussed is HIF1A; the disease is Sepsis.