In our laboratory, much interest has been generated after finding that morbidly obese subjects with low insulin resistance had higher adipose tissue VEGF-A levels than obese subjects with high insulin resistance, hypothesizing that upregulation of VEGF-A in adipose tissue could have a relationship with IR, believing that its upregulation is a compensatory mechanism that replaces the reduction in VEGF-B, VEGF-C, and VEGF-D [101]. This evidence concerns the gene VEGFC and Insulin resistance.