This is consistent with observations from other studies that fibulin family members are involved in cardiac fibrosis and reinforces the importance of fibulins as matricellular proteins in the development of fibrosis.[22, 39, 40] Therapeutic strategies attenuating cardiac fibrosis may disrupt optimal infarct (scar) formation, leading to post‐MI rupture.[41] But the loss of FBLN7 had little effect on post‐MI mortality in the study, suggesting that FBLN7 deletion ameliorated myocardial fibrosis in post‐MI mice without compromising infarct healing. Here, FBLN7 is linked to Myocardial fibrosis.