We demonstrated that (i) antagonisation of PROKR2 attenuated PE‐mediated hypertension and proteinuria, (ii) STE placentas and foetuses exhibited better outcomes in response to PKRA, (iii) the secretome of STOX1‐trophoblasts impacted the integrity of the fetal vasculature that was attenuated by PKRA treatment. The gene discussed is PROKR2; the disease is hypertensive disorder.