In MI mice, exchange protein activated by cyclic-adenosine, which could be upregulated by β-AR activation, prevents left atrial fibrosis (Surinkaew et al., 2019), while β-AR mainly modulates collagen production by CFs and causes proliferation of human CFs and fibrotic remodeling (Turner et al., 2003; Humeres and Frangogiannis, 2019). The gene discussed is ADRB2; the disease is myocardial infarction.