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.