Consequentially, reductions in transcript and protein expression for Nav1.5, Navβ1, and Kv4.3 are observed as an outcome of miR-34b/c targeting to seed regions present in the 3’-UTR of these genes, allowing KChIP2 to manipulate functional expression of a host of critical cardiac ion channel genes, ultimately acting as a key regulator of cardiac excitability and arrhythmia susceptibility. The gene discussed is KCND3; the disease is Arrhythmia.