As it is well known that HIF1a acting as a key pro-angiogenic transcriptional factor activated by hypoxia and translocated to the nucleus to induce the production of several endothelial growth factors, a recent study reported that miR-182, a member of miR-96/182/183 cluster, directly suppresses the expression of prolyl hydroxylase domain enzymes (PHD) and the inhibiting factor HIF-1 (FIH1) in prostatic tumor cells causing a marked increase in HIF1a activity (Li et al., 2015). Here, HIF1A is linked to prostate neoplasm.