Of interest, previous studies showed that in breast cancer, HIF1‐α induction upon hypoxia might be a crucial modulator of PRC2 function through selectively suppressing SUZ12 and EED, leading to a functional switch toward EZH2/FoxM1‐dependent induction of cell invasiveness66; and reportedly, HIF‐1α was overexpressed in preeclamptic placenta and involved in mutant trophoblast differentiation through transactivating TGF‐β3 promoter activity and elevating endogenous TGF‐β3 expression.67 This evidence concerns the gene EED and breast cancer.