Annotations out of the diagonal corresponding to differential expression in healthy controls (controls), patients with non-COVID-19 ARDS (ARDS) or patients with COVID-19 (COVID) are indicated. It was rapidly recognised, after the start of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) pandemic in December 2019, that only a minority of patients with coronavirus disease 2019 (COVID-19) develop severe or critical disease, while most SARS-CoV-2-infected patients are either asymptomatic or exhibit mild symptoms.1 Patients with severe COVID-19 may present life-threatening acute respiratory distress syndrome (ARDS) resulting from lower respiratory tract disease, associated with excessive inflammatory response, high pro-inflammatory cytokine production (cytokine storm) and coagulopathy.2 Several comorbidities, including hypertension, diabetes, cardiovascular disease and respiratory disease, have been associated with poorer prognosis and increased mortality.3 Increasing evidence suggests that neutrophils, a principal effector of the immune defence in airway infections, may play a major role in severe COVID-19 disease pathophysiology. In addition, we detected higher levels of proteins involved in chromosome condensation and segregation belonging to the condensin and the structural maintenance of chromosome (SMC) protein complexes in patients with COVID-19 and patients with non-COVID-19 ARDS, compared to healthy controls (Figure 2D). [Extracted from the article]