In this issue of the JCI, Tang et al. show that neutrophil extracellular trap (NET) formation contributes to cardiac hypertrophy and dysfunction in a mouse model of angiotensin II–induced cardiomyopathy, and that Krüppel-like factor 2 (KLF2) functions in neutrophils to oppose this process. This evidence concerns the gene AGT and cardiomyopathy.