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 The gene discussed is EZH2; the disease is breast cancer.