PAR4 activation elicited a rapid and sustained phosphorylation of CaMKII at Thr287, which is causally linked with NLRP3 inflammasome activation in atrial cardiomyocytes and the vulnerable AF substrate (Heijman et al. 2020), and of mTOR and AKT, which are functionally linked with CaMKII activation (Dong et al. 2019, Fan et al. 2021), as well as NLRP3 inflammasome activity and autophagic redox stress in atrial cardiomyocytes (Bairashevskaia et al. 2022, Lu et al. 2024). This evidence concerns the gene AKT1 and atrial fibrillation.