Coronavirus disease in 2019 (COVID-19), as caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been associated with significant morbidity and mortality worldwide. Although SARS-CoV-2 primarily targets the respiratory system, it can cause various hematological and hemostatic derangements, most notably coagulopathies in severe cases. 1, 4 Thrombocytopenia and elevations in fibrinogen and D-dimer have been reported to be prognostic indicators of COVID-19 severity and/or mortality. 2, 4 Changes in hemostatic parameters correlate with parallel rises in inflammatory markers such as cytokines and C-reactive protein (CRP). 4 Key mechanisms for SARS-CoV-2–induced coagulopathy include severe lung injury, alterations in the renin–angiotensin–aldosterone system (RAAS), and overactivation of the immune inflammatory pathways. 3, 4

Of relevance to the current commentary, certain demographic and clinical factors, such as older age and preexisting comorbid conditions, can increase the risk of more severe infections. 5, 6 The number of COVID-19 cases is similar among males and females, as evidenced by data from over 700,000 confirmed COVID-19 cases collected by the World Health Organization (WHO). 7 However, a recent meta-analysis suggests that men are more likely to experience severe disease and mortality compared with women. 8 Yet, it is unclear whether the disparities in COVID-19 clinical outcomes are due to underlying sex-based biologic differences or gender-based behavioral differences. Exploration of the sex-and gender-based differences in SARS CoV-2 infection is vital, as these may carry potential implications for disease progression, outcome severity, vaccine response, therapeutic intervention and effectiveness, recruitment of males and/or