Due to endothelial barrier dysfunction that allows T cell trafficking into the lung tissues autopsied from deceased COVID-19 patients [15] as well as acute lung injury reported in murine models of COVID-19 subjected to S1 protein [16], we next assessed whether the S1 protein without all the remaining viral components is sufficient to cause endothelial barrier disruption by growing HPAEC in a tight monolayer and monitoring for changes in endothelial permeability by measuring the passage of FITC conjugated-dextran (40 kD) through the monolayers [17,18]. The gene discussed is PSMD1; the disease is COVID-19.