The same group, in 2018 [48], found that deletion of either Tet2 or Dnmt3A in bone marrow caused increased cardiac hypertrophy and fibrosis and a reduction in cardiac function in mice with angiotensin-II-induced HF, suggesting that the reduced survival rate seen in patients with TET2 or DNMT3A mutations is causally related to altered immune cell function in the myocardium [39,40]. This evidence concerns the gene DNMT3A and cardiac hypertrophy.