As an example, increased platelet-monocyte aggregate formation has been described to trigger TF expression and immunothrombosis in critically ill COVID-19 patients (Hottz et al., 2020; Manne et al., 2020; Zaid et al., 2020), whereas other studies found diminished levels of circulating platelet-leukocyte aggregates in fatally ill patients, linked to a hypo-responsive platelet phenotype with impaired GPIIb/IIIa activation (Schrottmaier et al., 2021). This evidence concerns the gene TF and COVID-19.