Mao et al. (2020) showed that PI3K–AKT–mTOR signaling was overactivated in a rat Takotsubo Syndrome (TTS) model established by ISO, implying the potential role of PI3K–AKT–mTOR signaling in the cardiac dysfunction induced by stress; they attributed the protection of chronic AKT inhibition against cardiac dysfunction of TTS rats to reduction of mitochondrial reactive oxygen species (ROS) and ROS‐induced apoptosis. The gene discussed is MTOR; the disease is Tako-tsubo cardiomyopathy.