Finally, CUL2 was chosen as a representative validation gene due to the strength of its intronic hMeSeal-seq peak and its function as a component of the tumor-suppressive Von Hippel-Lindau complex, inhibiting uncontrolled angiogenesis via ubiquitination and degradation of hypoxia-inducible factor 1 alpha (HIF1α) [48]. This evidence concerns the gene HIF1A and neoplasm.