Using these methods, supported by in silico studies, immunohistochemistry and biophysical data, we have provided evidence for the previously unrecognized presence of gap junction gamma-3 protein in arteries from patients with ischaemic heart disease and interaction of simvastatin and fluvastatin hydroxyacids with the N-terminal sequence of this human gap junction gamma-3 protein. The gene discussed is GJC3; the disease is heart disorder.