This study further confirms that the proosmotic functions of miR-22-3p are attributed to the direct suppression of the secreted antiosmotic factor VE-cadherin within ECs, which may suggest one mechanism of the upregulation of miR-22-3p increasing the endothelial permeability in CRSwNP. This evidence concerns the gene CDH5 and chronic rhinosinusitis with nasal polyps.