Subjects in the CAD group exhibited a significantly higher variant burden than those in the CAD-free group (72-89 years old), both in terms of the total number of somatic variants and disruptive variants affecting protein function (with significant change in DNMT3A and second most effected was TET2) (Kwiatkowska et al., 2025). The gene discussed is TET2; the disease is coronary artery disorder.