Alternatively, fibronectin–integrin interactions play a key role in maintaining endothelial barrier function during sepsis (15, 16, 92, 93, 94, 95), which may be disrupted by competition from spike protein fragments during SARS-CoV-2-driven inflammation, a hypothesis that is supported by recent work in vascular endothelial cells (35). The gene discussed is FN1; the disease is Sepsis.