Under physiological conditions, TP53 is functionally active to maintain cardiac structure, but elevated TP53 expression can lead to myocardial fibrosis, myocardial hypertrophy, myocyte apoptosis, non-myocyte proliferation, and left ventricular dilation leading to cardiac dysfunction.[22] Therefore, inhibition of TP53 may serve as one of the effective therapeutic strategies to prevent the transition from cardiac hypertrophy to HF. This evidence concerns the gene TP53 and Myocardial fibrosis.