Importantly, we observed significantly elevated TAK1, JNK1/2 and p38 phosphorylation levels, along with increased ANP and β-MHC, in heart samples from DCM and HCM patients compared with those of normal controls, indicating a close association between TRAF6 and the TAK1-JNK1/2/p38 axis during the clinical development of cardiac remodelling (Fig. 7a). The gene discussed is MAP3K7; the disease is familial dilated cardiomyopathy.