When investigating the reoccurrence of fetal splicing variants of fibronectin in cardiovascular diseases, one could learn that especially the extra domain A of fibronectin (ED-A+ Fn) can be frequently detected in diseased cardiac tissue from patients with ischemic cardiomyopathy, valvular heart disease, and dilated cardiomyopathy and also in a rat model of chronic cardiac rejection by our group [25–30]. This evidence concerns the gene FN1 and ischemic cardiomyopathy.