Importantly, the growth of visceral fat and expansion of white adipose tissue associated with obesity results in a hypoxic environment that activates increased levels of HIF1-α which in turn increases VEGF-A to stimulate angiogenesis and support rapid growth of adipose tissue, but also leads to an upregulation of inflammatory adipokines and promotes tissue fibrosis leading to adipose tissue dysfunction (Rutkowski et al., 2009). This evidence concerns the gene VEGFA and obesity disorder.