STIM1 in vitro deletion was associated with agonist-inducedhypertrophy inhibition, whereas STIM1 silencing in vivo prevents thePO-induced hypertrophy development but can also reverse preestablished CH, thoughburdened by a rapid HF onset, mainly through mTORC2–AKT–GSK3β pathway[110, 111]. Here, AKT1 is linked to hydrops fetalis.