Multiple studies reported that increased expression of miR-21 in fibroblasts of the failing heart induces the extent of interstitial fibrosis and cardiac hypertrophy by augmenting ERK–MAP kinase activity via inhibition of sprouty homolog 1 (Spry1) (91) or enhancing matrix metalloproteinase-2 (MMP-2) via PTEN (phosphatase and tensin homolog) pathway (92). The gene discussed is MMP2; the disease is cardiac hypertrophy.