These results suggest that PI16 produced by CMs cannot directly attenuate Ang II–induced cardiac hypertrophy, which meet the hypothesis in recent studies that although PI16 exists in cardiac myocytes and is able to modulate their hypertrophic response, the dominant effects of PI16 on cardiac function may originate from the cardiac fibroblasts.12, 15. This evidence concerns the gene PI16 and cardiac hypertrophy.