For instance, either overexpression of constitutively active or dominant negative forms of MKK3/6 in vitro result in cardiac hypertrophy (Braz et al., 2003; Streicher et al., 2010; Zechner et al., 1997), while in vivo transgenic overexpression of MKK6 in mouse heart did not affect cardiac hypertrophy but resulted in protection against myocardial infarction and reduced levels of markers of apoptosis (Martindale et al., 2005). The gene discussed is MAP2K6; the disease is cardiac hypertrophy.