AKT1 and neoplasm: Irreversible activation of the HIF-1α-related pathway via stimulation by the initial activation of HIF-1α due to hypoxia and PTEN/PI3K/Akt activation, the HIF-1α-induced overexpression of miR-182, and the resultant limited PHD2 and FIH1 expression due to miR-182 overexpression eventually results in HIF-1α protein accumulation as well, facilitating angiogenesis and tumor growth in prostate cancer [170].