Meg3 was known to act as a transcriptional regulator of gene expression,recruiting and guiding chromatin remodelling complexes to target sites [132, 133].In 2017, it was identified as a regulator of the expression of thefibrosis-related gene matrix metalloproteinase-2 (MMP2) in CFs through therecruitment of p53, this latter induced by TGF-β signalling; moreover,Meg3 silencing in vivo after TAC decreased myocardial fibrosis andimproved diastolic function, thus revealing a new potential target for theprevention of pathological remodelling in heart diseases [131]. This evidence concerns the gene MMP2 and Myocardial fibrosis.