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. This evidence concerns the gene AKT1 and Tako-tsubo cardiomyopathy.