Early-stage studies ruled out the phosphatidylinositol 3-kinase-protein kinase B (PI3K-Akt) signaling pathway, a critical downstream effector of B-cell receptor signaling in the treatment of blood malignancies, as the underlying mechanism for ibrutinib-related AF (McMullen et al., 2014; Pretorius et al., 2009). This evidence concerns the gene AKT1 and atrial fibrillation.