NFE2L2 and hydrops fetalis: The ability of AEOL to limit infarct expansion, adverse LV remodeling, and HF progression was abolished byNrf2gene knockout; moreover, AEOL-induced NRF2 activation upregulated the expression of the micropeptide DWORF, a potent regulator of myocardial contractility via enhanced SERCA2a activity (Mbikou et al. 2020), achieved by displacing the SERCA-2a inhibitor PLN.