Although studies comparing and contrasting activities of TGFBI and periostin head-to-head are sparse, TGFBI and periostin were recently found to act similarly in the heart in affecting fibrosis and disease responsiveness; however, TGFBI is seemingly not necessary in the heart after myocardial infarction injury and is fully compensated by the more prominently expressed effector periostin [12]. Here, TGFBI is linked to myocardial infarction.