Col15a1‐deficient mice exhibit non‐proto‐fibrillar protein deposits in the cardiac myocardium interstitium, along with an abnormal increase in the Col1a1/Col3a1 ratio, heightened myocardial stiffness, reduced elasticity, and decreased myocardial compliance, ultimately leading to cardiomyopathy [20]. This evidence concerns the gene COL3A1 and cardiomyopathy.