In conspectus of (I) the attenuated BNP/NPR-A/cGMP pathway in LM of HF animals, (II) the published link between natriuretic peptide signalling and PGC-1α expression and (III) histological, transcriptomic and proteomic hallmarks of reduced PGC-1α activity, we hypothesised that a pharmacological intervention, increasing the availability of biological active BNP without aggravating effector desensitization[15], increases PGC-1α expression and thus, ameliorates protein content of skeletal muscle as surrogate marker of catabolic dominance and clinically, cachexia. The gene discussed is NPR1; the disease is Cachexia.