Several authors have demonstrated accumulation of hypoxia inducible factor 1α (HIF-1α) and HIF-2α within HLRCC tumors leading to increased vascular density in uterine leiomyomas as well as an increase in glucose transporter 1 (GLUT1) in HLRCC kidney tumors [4, 5]. This evidence concerns the gene HIF1A and hereditary leiomyomatosis and renal cell cancer.