COPD makes CHIP less indeterminate

In this issue of Blood, Miller and colleagues convincingly demonstrated the contribution of clonal hematopoiesis of indeterminate potential (CHIP) to the risk of chronic obstructive pulmonary disease (COPD).(1) Their epidemiological data are supported with a transgenic mouse study showing that mice with Tet2-deficient hematopoietic cells, used as a model for CHIP, have increased airway inflammation and an increased risk for emphysema after various stimuli.