FH and hereditary leiomyomatosis and renal cell cancer: Molecular investigations of HLRCC may provide insight into the etiology of ULMs and tumorigenesis that includes deleterious mutations of FH as this alteration results in mitochondrial dysfunction and energy depletion, which can promote DNA damage as a product of elevated free radicals and activation of hypoxia-responsive signal transduction pathways that can further lead to angiogenesis and growth factor production8,9.