The decreased ratio between COL3A1 and COL1A1 expression suggested that, in all conditions, there was a superior accumulation of new Collagen Type I respect to Collagen Type III (Figure 2f), which is typical hallmark of the last stages of post‐infarction cardiac fibrosis, as highlighted in previous studies and in clinical reports.[18] The role of both TGF‐β1 and mechanical stretching in triggering ECM production was also confirmed by the analysis of deposited Collagen Type I, Fibronectin and Aggrecan proteins (Figure 3). The gene discussed is COL3A1; the disease is infarction.