Notably, MAPKAPK5 may influence AF via MAM-dependent mechanisms: Studies show that targeting MAPK pathways mitigates atrial remodeling: SMLC inhibits oxidative stress through the MsrA/p38 MAPK axis, protecting against atrial-ventricular remodeling in AF (Xu et al., 2024); α-BTX, an α7nAChR antagonist, suppresses the oxi-CaMKII/MAPK/AP-1 pathway to normalize calcium handling, alleviating mitochondrial dysfunction, apoptosis, and atrial fibrosis in AF models (Zhao et al., 2023). The gene discussed is CAMK2G; the disease is atrial fibrillation.