Although our results showed that Rac2/cofilin played a crucial role in actin cytoskeleton disarray induced by RVOT bigeminy VPC, the role of other aforementioned pathways or mechanisms which possibly involve channelopathy, beta-adrenergic receptors, and so on, in VPC-induced cardiomyopathy was not well elucidated and merits further study. The gene discussed is RAC2; the disease is channelopathy.