Our data are consistent with a study conducted by Strohmeier et al. 2022 that showed a decrease in endothelial adherens (VE-cadherin) and tight junction (ZO-1) gene expression in healthy human primary ECs treated with CM derived from lipedema SVF, confirming the increase in the endothelial permeability and leakiness of ECs; thus, endothelial barrier dysfunction [60]. The gene discussed is CDH5; the disease is Lipedema.