The COVID-19 pandemic, caused by the spread of severe acute respiratory syndrome coronavirus 2, has resulted in more than 1· 8 million deaths worldwide as of Jan 7, 2021, a figure that will grow indefinitely until effective vaccines become globally accessible. Two phases are generally recognised in the pathogenesis of COVID-19: an initial viral stage characterised by an appropriate host immune response, mild clinical symptoms, and self-resolution in most patients; and a later phase develops in a minority of patients, and is characterised by maladaptive hyperinflammation, rampant release of cytokines, acute respiratory insufficiency, and considerable mortality. Dampening hyperinflammation in patients with severe COVID-19 via inhibition of cytokines has emerged as a logical therapeutic option. 1

Corticosteroids, which non-selectively inhibit cytokine production, were assessed in the RECOVERY trial and found to moderately reduce mortality compared with usual care alone in patients with moderate-to-severe COVID-19. 2 Among targeted cytokine inhibitors, IL-6 and IL-1 inhibitors have attracted a lot of clinical attention, for instance in cohort studies of severe COVID-19 IL-1 inhibition with anakinra improved clinical outcomes, 3 whereas IL-6 inhibition yielded more conflicting results. 4 Eventually, controlled evidence became available that IL-6 inhibition is marginally or not effective for COVID-19, 5 which left anakinra as the main candidate among targeted cytokine inhibitors. However, the efficacy of anakinra in COVID-19 had not been tested in controlled settings.