Clonal hematopoiesis of indeterminate potential (CHIP) refers to a population of myeloid stem cells with acquired gene mutations, but does not fulfill the diagnostic criteria for hematologic malignancy.1 There is growing evidence supporting the role of CHIP mutations in altered immune function through effector cells such as monocytes/macrophages and their dysregulated cytokine/chemokine expression.2,3 Since the immunopathogenesis of such an adverse outcome of CHIP largely shares that of severe COVID-19,4 such as high levels of circulating pronflammatory cytokines or dysregulated monocytes and macrophages,5,6 several previous studies have examined whether CHIP might contribute to the progression of COVID-19.7- 9 However, due to the weak significance of association or lack of stratified analysis, it is still unknown whether the presence of CHIP in previously healthy COVID-19 patients has a clinical impact on the disease severity. In this study, we aimed to verify the clinical implications of CHIP in COVID-19 severity, especially in patients without canonical clinical risk factors for severe COVID-19 by analyzing clinical and laboratory characteristics using clustering and statistical examinations including interaction term.