In the same context of use, Tranilast, an antihistamine suppressing the expression and activity of TGFβ that was initially developed to treat bronchial asthma and that was found effective in cardiomyopathy animal models,[51] significantly reduced both myofibroblasts transition and ECM deposition (Figure 4d), as observed through immunofluorescence staining of α‐SMA, Collagen type I, Fibronectin and Aggrecan. The gene discussed is FN1; the disease is cardiomyopathy.