The past year has demonstrated the power of collaborative scientific effort in rapidly developed vaccines to curb the SARS-CoV-2 pandemic and repurposed drugs to improve patient outcomes in severe COVID-19 disease. The morbidity and mortality associated with COVID-19 remains significant, however. Better understanding of COVID-19 pathogenesis will aid future therapeutic advances. Viral infection first triggers the innate immune system, with stimulation of natural killer cells and dendritic cells, secretion of interferon and presentation of viral antigens to the adaptive immune system, which mounts a specific antibody and T lymphocyte response towards the virus and develops memory against it. However, a recent study published in Blood by Althaus et al. shows that in COVID-19, the antibody arm of the adaptive immune response also triggers platelet procoagulant activity, thereby exacerbating the disease.