Although the endothelial precursors were higher in the AT of the obese patients compared to lean controls (Fig. 4D,E), they seemed to be unable to differentiate into mature endothelial cells or to form capillary structures (Figs 1D,E and 4F,G), suggesting that HIF1A upregulation during obesity induces only a detrimental transcriptional program contributing to AT dysfunction17,19,20,23. This evidence concerns the gene HIF1A and Obesity.