An indication that angiogenesis in uterine fibroids could follow a different trajectory from the normal hypoxia response—with HIF-1α stabilization and the expression of VEGF as a result, which in turn induces sprouting and outgrowth of endothelial cells nearby to establish a connection to vascular supply (77)—was the finding that despite their hypoxic state, uterine fibroids surprisingly show a down-regulation of key players of the normal hypoxic response, HIF-1α for example has been shown lacking in uterine fibroids, when it was readily shown in leiomyosarcomata (78, 79). The gene discussed is HIF1A; the disease is uterine corpus leiomyoma.