Recognition that molecular (or epitope) mimicry is more widespread in RHD/AM helps to resolve one problem – how intracellular proteins such as myosin become targets in RHD/AM – but exacerbates another, which is that laminins, collagens, and even DAF and CAR are fairly widespread proteins that are certainly not limited to cardiac tissue. This evidence concerns the gene LAMB2 and rheumatic heart disease.