Moreover, investigations in diabetic cardiomyopathy (DCM) models have shown that the loss of natriuretic peptide receptor C (NPRC) in both DCM mice and patient myocardia upregulates TGF-β-induced factor homeobox 1 (TGIF1); consequently, TGIF1 inhibits Smad2/3 phosphorylation, thereby attenuating cardiac fibrosis and improving remodelling and function in diabetic mice (6). Here, SMAD2 is linked to familial dilated cardiomyopathy.