On the other hand, the silencing of TRAF6 reduces the phosphorylation levels of JNK1/2 and p38 in the hypertrophied heart.63, 64 These findings reveal that oxidative stress‐induced activation of ubiquitin E3 ligases such as TRAF6 plays an active role in the development of pathological cardiac hypertrophy. Here, PRKN is linked to cardiac hypertrophy.