An animal study of CKD by Winterberg et al. identified that T cells, especially IFNγ+ CD4+ T cells, infiltrated the heart and led to diastolic dysfunction, whereas depletion of T cells significantly ameliorated diastolic function without altering left ventricular hypertrophy, hypertension or renal dysfunction, suggesting a causal role for T cells in diastolic dysfunction during UCM (20). The gene discussed is CD4; the disease is hypertensive disorder.