Specifically, FTO mitigates cardiac dysfunction in pressure overload-induced HF mice through modulating glycolysis at least partially by removing phosphoglycerate mutase 2 (PGAM2) m6A and also modulating glucose uptake probably by regulating the protein kinase B (AKT)-glucose transporter type 4 (GLUT4) pathway [199]. The gene discussed is FTO; the disease is hydrops fetalis.