Clonal hematopoiesis (CH) is defined by acquired mutations in leukemia driver genes within the hematopoietic stem- and progenitor cells, which provides these cells with a growth advantage over the wild type cells, resulting in clonal expansion. CH is detected in the peripheral blood of >30% of older individuals (above 60 years) and the prevalence increases up to 50% in elderly above 80 years old. The presence of CH associates with an increased morbidity and all-cause mortality and a tenfold increased risk of developing leukemia. Mutations in DNMT3A and TET2, both involved in the DNA methylation pathway, are identified in approximately 80% of the individuals with CH mutations. While DNMT3A functions as a methyltransferase, TET2 plays a role in the active hydroxylation and demethylation of 5-methylcytosines. Studies have shown that mutant TET2 cells may contribute to localized hyperinflammation, increasing the risk of developing cardiovascular disease. We have previously shown that individuals who carry mutations in TET2 are significantly more likely to acquire additional mutations in either TET2 or SRSF2, and the presence of TET2 mutations significantly elevates the risk of developing hematological malignancies. Here, we aim to further characterize individuals with CH and TET2 mutations, their co-mutations, expansion rate and the risk of adverse events.