Because mice do not typically develop spontaneous AF, elicitation requires electrical stimulation and alterations such as obesity or atherosclerosis-promoting diets.17,20,28–30 As an initial step, we examined the effect of Tet2 inactivation in hematopoietic cells in atherosclerosis-prone Ldlr−/− recipient mice.3,4 Lethally irradiated Ldlr−/− (CD45.1) mice were transplanted with bone marrow with hematopoietic-specific inactivation of Tet2 (Tet2fl/−Vav1-Cre+ CD45.2, or Tet2 knockout [Tet2KO]) or WT (Vav1-Cre+ CD45.2 or WT) control. The gene discussed is LDLR; the disease is atrial fibrillation.