In a mouse model of heart failure, reductions of Ito in ventricular myocytes is primarily due to reduction in a pore-forming α-subunit Kv4.2 and less so for Kv4.3 α-subunit38 while reduced expression of the associated β-subunit KChIP2 has been reported to be responsible for the reduction in Ito noted in human heart failure and in a mouse model of hypertrophy39–41. This evidence concerns the gene KCND2 and heart failure.