This fits well with recent data in a cardiomyocyte-specific NPR-B−/− strain that exhibits a negligible intrinsic phenotype in response to pressure overload,33 diminished ventricular expression of NPR-B in HF patients (albeit not recapitulated herein),7 impaired sinoatrial conduction and aggravated atrial fibrosis in NPR-C−/− mice,28 and a human NPR-C genetic variant that precipitates LV dysfunction.34 This evidence concerns the gene NPR3 and hydrops fetalis.