The mechanisms of atrial fibrillation associated with ibrutinib and other BTK inhibitors involve the inhibition of C-terminal Src kinase (CSK), enriched in the atria, as well as the inhibition of the PI3K/AKT and ion channel pathways, potentially enhancing Ca2+/calmodulin-dependent protein kinase II (CaMKII) [151]. This evidence concerns the gene CSK and atrial fibrillation.