This finding confirms recent work by Biancatelli et al. [16], indicating the S1 protein alone is capable of inducing barrier dysfunction in human pulmonary microvascular cells and is notable given that HPAEC represent a substantial amount of all lung endothelial alveolar cells and provide a possible mechanistic basis for understanding why the lungs are a target organ for immune-mediated destruction in COVID-19 patients [35]. This evidence concerns the gene PSMD1 and COVID-19.