A post-MI study demonstrated that WNT pathway activity contributes to cardiac fibrosis by expanding αSMA-positive myofibroblasts.101 This is in line with increased expression of markers like SNAI2.102 Additionally, an independent study showed that inhibition of WNT signalling via the secreted frizzled-related protein 3 (sFRP3) blocks EndMT in mitral valves post-MI. This evidence concerns the gene FRZB and myocardial infarction.