Our future studies will focus on deciphering the role the cleavage and inactivation of MEK proteins may or may not play in LT-induced cardiomyopathy, the molecular mechanism of LT-induced early cardiac damage, the means by which nNOS-derived NO is protective against LT effects and the tissue sites at which nNOS manifests these effects. This evidence concerns the gene MAP2K7 and cardiomyopathy.