In a stunningly short period of time, the unexpected coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has turned the unprepared world topsy-turvy . Although the rapidity with which the virus struck was indeed overwhelming, scientists throughout the world have also been up to the task of deciphering the mechanisms by which SARS-CoV-2 induces the multisystem- and multiorgan-inflammatory response that, collectively, contribute to the high mortality rate in affected individuals . In this issue of the JCI, Skendros et al., is one such team who report that the complement system plays a substantial role in creating the hyper-inflammation and thrombotic microangiopathy that appear to contribute to the severity of COVID-19 . In support of the hypothesis that the complement system along with neutrophils and platelets contributes to COVID-19, the authors presented empirical evidence showing that treatment with the complement inhibitor, compstatin Cp-40, inhibited the expression of tissue factor in neutrophils . These results confirm that the complement axis plays a critical role and suggests that targeted therapy using complement inhibitors is a potential therapeutic option to treat COVID-19 induced inflammation.