Early in the COVID-19 pandemic it was noted that a subset of people with severe disease were admitted to hospital with a hyperinflammatory illness.Subsequently, trials investigating immunomodulation as a treatment for severe COVID-19 resulted in dexamethasone becoming standard of care for people admitted to hospital with severe COVID-19 and the interleukin (IL)-6 receptor inhibitor tocilizumab being recommended for people requiring supplemental oxygen and with evidence of a significant inflammatory response. The clinical character, pathophysiology, and phenotype of hyperinflammation in severe COVID-19 is still being elucidated. The hypercytokinaemaia and hyperferritinaemia observed in COVID-19 is modest compared with the prototype cytokine storm syndromes haemophagocytic lymphohistiocytosis and macrophage activation syndrome. Instead, a model of more limited, lung-centric immunothr ombogenic inflammatory pathology has been proposed