This observation is explained by the hypothesis of “ADPN resistance” in which a reduction of ADPN receptors at the tissue level could be responsible for the lack of the ADPN protective effects.19, 20, 21 In cardiomyocytes isolated from C57/BL6 mice, AdipoR1, AdipoR2, and T-cad were significantly reduced after 4 to 8 weeks postmyocardial infarction, suggesting that an altered receptor expression might be responsible for impaired ADPN signaling in late HF stages.29 The gene discussed is ADIPOR2; the disease is hydrops fetalis.