While the most commonly mutated genes in lung recipients with CHIP were the epigenetic regulators DNMT3A and TET2, the proportion of mutations in DNMT3A (11%) and TET2 (9%) in our cohort was much lower than prior studies of patients with heart failure [41], coronary heart disease [6], COPD [42], and healthy volunteers [7], where about 70% of variants were in DNMT3A or TET2. Studies in cardiovascular disease suggest adverse events associated with CHIP are driven by TET2 and DNMT3A [34, 35]. Here, TET2 is linked to chronic obstructive pulmonary disease.