In AF model mice induced by Ach-CaCl2, the hyperactivation of ERK1/2 and AKT /mTOR signaling not only improve the survival of cardiomyocytes but also synchronously stimulate the proliferation and hypertrophy of and collagen production by cardiac fibroblasts aggravating atrial fibrosis and providing substrate for AF [55]. The gene discussed is MTOR; the disease is atrial fibrillation.