Clonal hematopoiesis (CH) is a phenomenon in which hematopoietic stem cells carry genetic mutations with advantageous growth potential, resulting in aberrant expansion of immature and mature hematopoietic cell populations over time.1,2 Loss-of-function heterozygous mutations in TET2 (tet methylcytosine dioxygenase 2) are among the most prevalent and significant drivers of CH and myelodysplastic syndromes, an age-related hematological disease.3 In addition, certain diseases, or environmental conditions, for example, atherosclerosis drive the onset and trajectory of TET2 deficiency-related CH (TedCH).4 Our previous study suggest inflammation play a positive role in driving TedCH. To further explore the potential drivers of CH (i.e. LPS-induced inflammation), we assessed the impact of another four different environmental factors on TedCH and confirmed that accelerated TedCH depends on the establishment of an inflammatory environment (here colitis-induced).5