In most individuals, infection with SARS-CoV-2 is either asymptomatic or produces mild illness (COVID-19) that resolves spontaneously; yet, a small proportion of patients with COVID-19 develop severe disease, require hospitalisation (often in a critical-care setting), and die.1 A dysregulated type I interferon response to SARS-CoV-2 with overproduction of proinflammatory cytokines seems to be a key pathogenic mechanism underlying progression to severe COVID-19 and death.1 Thus, controlling this excessive inflammatory response might potentially prevent disease progression.