The PI3K/AKT axis critically modulates normal physiological processes, including cell survival, proliferation, growth, apoptosis, and angiogenesis.33 Modulation of the PI3K/Akt pathway has been shown to mitigate myocardial fibrosis and remodelling caused by diabetes, isoproterenol, and other factors.34 Chronic activation of AKT is deleterious, with prolonged overexpression of AKT in HF leading to cardiac fibrosis and pathological hypertrophy. Here, AKT1 is linked to hydrops fetalis.