revealed that based on the mutual inhibitory relationship in the HIF-1α-DNM2 and HIF-1α-miR-199a interaction, dynamin 2 (DNM2), HIF-1α and miR-199a, which arises from the opposite strand of the DNM2 gene, are integrated into a feedback loop, which increases both the posttranscriptional level and protein stability of HIF-1α to promote ovarian cancer metastasis [162], and reciprocal suppression between miR-20b and HIF-1α at the transcriptional and posttranscriptional levels also plays a role in fine-tuning the adaptation of tumor cells to different oxygen concentrations [163]. The gene discussed is HIF1A; the disease is ovarian cancer.