Our study found that the incidence of atrial fibrillation-related fatality was relatively higher in ibrutinib after its long-term time use; the underlying pathogenetic mechanism may be due to its inhibitory effect on multiple kinases, including ERBB2 and the PI3K-AKT pathway, resulting in the off-target effects of ibrutinib at its therapeutic concentration (McMullen et al., 2014; Tenin et al., 2014). The gene discussed is ERBB2; the disease is atrial fibrillation.