Since intermittent hypoxia (IH)-induced alterations in tumor malignancy are driven, at least in part, by the transcriptional activity of hypoxia inducible factor-1α (HIF-1α) pathways (5–7), it is not surprising that many of the HIF-1α genes that are involved in regulation of cellular bioenergetics, angiogenesis, and expansion of the vascular supply network exhibit increased expression within rapidly proliferating tumors and are, therefore, considered as potentially viable reporters of CM aggressiveness and poor outcomes (8, 9). Here, HIF1A is linked to neoplasm.