During cardiac fibrosis, proliferated CFs act as an important contributor.[37, 38] It has been previously reported that cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non‐myocyte proliferation and requires TGF‐β.[6] Indeed, there is an abundant CFs in the myocardial interstitial area after ISO treatment, accompanied by a significant upregulation of TGF‐β1 in the CMs. The gene discussed is TGFB1; the disease is hypertrophic cardiomyopathy.