Importantly, Manso AM et al. found that the level of Tln1 was upregulated in human failing heart and in the TAC mouse model, and demonstrated that the specific knockout of Tln1 in cardiomyocytes showed blunted hypertrophy, less fibrosis, and improved cardiac function by inhibiting the activation of ERK1/2, p38, Akt, and glycogen synthase kinase 3 in mechanical overload mice model [34]. This evidence concerns the gene TLN1 and persistent truncus arteriosus.