Next, we sought to determine whether lentivirus-mediated Cx43 transduction of SKM results in formation of functional gap junctions in vivo and hence post-MI VT protection equivalent to our earlier studies indicating that engraftment of SkM harvested from transgenic mice overexpressing Cx43 under control of a SkM promoter protected against post-MI VT in vivo. The gene discussed is GJA1; the disease is myocardial infarction.