TET2 and coronary artery disorder: Although inflammation represents a common mechanism involved in both HFpEF and HFrEF, chronic inflammation and fibrotic remodeling driven by myeloid cells is increasingly recognized as a primary contributor to HFpEF.20 Animal models of CHIP, particularly TET2 CHIP, support a role for CHIP-induced inflammatory dysregulation in the pathogenesis of cardiac remodeling, fibrosis, and ventricular dysfunction.4,5,6 Post-hoc analyses from the CANTOS trial21 suggested that individuals with TET2 CHIP may derive particular benefit from interleukin-1β inhibition to reduce risk of CAD.