In a recent study, syndecan-4−/− mice were shown to have impaired cardiac function and increased mortality following myocardial infarction [46], while in another study, cardiac function was improved and NFAT activation increased in syndecan-4−/− mice after infarction [47], suggesting additional layers of complexity in syndecan-4-dependent NFAT regulation and remodeling of the heart. This evidence concerns the gene SDC4 and myocardial infarction.