All three genes were significantly more expressed in the hearts of fortilinKO-heart mice than in those of fortilinWT-heart mice at both message (Fig. 2e) and protein (Fig. 2f) levels, suggesting that the lack of fortilin in cardiomyocytes may lead to p53-induced transcriptional activation of these genes, leading to cardiomyocyte apoptosis and myocardial fibrosis. Here, TP53 is linked to Myocardial fibrosis.