In fact, this study reveals that ventricular specimens from HF patients and healthy controls have a predominant cardiomyocyte expression of NPR-C, whereas in failing hearts additional fibroblast localization is observed; such findings support the concept that CNP-dependent NPR-C activation on both cardiomyocytes and fibroblasts drives the cardioprotective actions of the peptide. The gene discussed is CNP; the disease is hydrops fetalis.