HIF3A and neoplasm: Given that DDIT4 function inhibits the mammalian target of rapamycin (mTOR) during stress, and DDIT4 expression promotes tumor cell apoptosis (Yang et al., 2018[40]), we next tested if HIF3A knockdown resulted in increased HUVECs survival as monitored by decreased caspase activity during hypoxia because of reduced DDIT4 expression.