AGT and cardiac hypertrophy: Moreover, genetic deletion in the myeloid compartment (including monocytes/macrophages and neutrophils) of Krüppel-like factor 2 (KLF2), a transcription factor that has been shown to oppose inflammation (8), increases neutrophil accumulation in the myocardium and enhances cardiac hypertrophy, fibrosis, and dysfunction upon angiotensin II infusion; notably, this cardiac phenotype was also suppressed by depleting neutrophils with anti-Ly6G antibody (6).