AimsAtrial fibrillation (AF) is the most common cardiac arrhythmia, and early-onset lone AF has been linked to mutations in genes encoding ion channels. Mutations in the pore forming subunit K4.3 leading to an increase in the transient outward potassium current (I) have previously been associated with the Brugada Syndrome. Here we aim to determine if mutations in K4.3 or in the auxiliary subunit K Channel-Interacting Protein (KChIP) 2 are associated with early-onset lone AF.Methods and resultsTwo hundred and nine unrelated early-onset lone AF patients (