Thus, it is tempting to speculate that an activated pro-inflammatory state in carriers of DNMT3A- and/or TET2-CHIP-driver mutations may have contributed to increased myocardial fibrosis in patients with severe AVS, which confers an increased risk for mortality even after successful removal of the obstructive valve by TAVR. The gene discussed is DNMT3A; the disease is Myocardial fibrosis.