FURIN, a protein that mediates proteolytic cleavage of non‐functional proBNP to its active hormone BNP, expressed at a significantly lower level in fibroblasts, endothelial cells, and macrophages from DCM than non‐failing hearts (Figure 6C), suggesting agonists of FURIN may help restore cardioprotective activity of BNP in DCM. The gene discussed is NPPB; the disease is familial dilated cardiomyopathy.