By using heart samples from HF patients and AMPKα2 genetically modified mouse models with transverse aortic constriction (TAC), researchers have found a serine residue (S495) in PINK1 that undergoes phosphorylation after exposure to AMPKα2 upon dissipation of the mitochondrial membrane potential in cardiomyocytes. Here, PINK1 is linked to hydrops fetalis.