Neurohumoral signaling, ischemic stress, inflammation, reactive oxygen species, and diabetes are all associated with activation of CaMKII resulting in cardiomyopathy and fibrosis (30, 39, 40), whereas specific profibrotic cytokines and neurohumoral factors such as AngII (41), interleukin-6 (42), tumor necrosis factor beta (17), and bone morphogenetic protein 4 (43) also provide CaMKII activation. This evidence concerns the gene LTA and cardiomyopathy.