In the study performed both in vivo with MI mice model and in vitro with CFs isolated from newborn pups, Huang et al. found that MALAT1 was specifically upregulated in MI heart and in AngII-stimulated CFs; knockdown of MALAT1 could alleviate cardiac fibrosis post-MI and AngII-induced fibroblast proliferation and collagen synthesis by suppressing TGF-β1 activity [74]. The gene discussed is MALAT1; the disease is myocardial infarction.