In mice treated with ibrutinib, a drug that increases the risk of AF development in cancer patients, there was an increase in ox-CaMKII, p-CaMKII (Thr-286), and p-RyR2 (Ser2814) expression, as well as increased SR Ca2+ leak, abnormal mitochondrial structures in atrial cardiomyocytes, atrial fibrosis, and pacing-induced AF [235,236]. This evidence concerns the gene CAMK2G and atrial fibrillation.