Apoptosis, which is characterized by cell shrinkage, plasma membrane blebbing, chromatin compaction and nuclear fragmentation, has been shown to participate in the pathogenesis of DCM.2 Recently, Li et al.14 demonstrated that H19/miR-675 axis was involved in the modulation of hyperglycemia-induced apoptosis by targeting VDAC1, which may provide a novel therapeutic strategy for DCM. Here, H19 is linked to familial dilated cardiomyopathy.