We identified an opposing relationship between HCM and DCM and the BNPs (both NT-proBNP and BNP); although the levels of BNPs are increased with the progression of both cardiomyopathies, causality via Mendelian randomization suggested that the BNPs are part of HCM pathology and progression, whereas the observed increase in DCM is an adaptive response to contractile dysfunction and cardiomyocyte stretch. The gene discussed is NPPB; the disease is familial dilated cardiomyopathy.