The prolongation of APD and significant delay in repolarization are closely related, which may increase the susceptibility to malignant arrhythmias through mechanisms such as triggered activity or re-entry.29 Cx43 is the main connexin found in ventricular gap junctions, and its deficiency is associated with slow and dispersed conduction.30,31 This study found that in ISO-induced HF mice, the protein expression of Cav1.2, Kv1.5, and Kv4.2 were significantly down-regulated, while overexpression of TNIP3 could reverse these adverse changes. The gene discussed is TNIP3; the disease is hydrops fetalis.