For example, cardiomyocyte-specific overexpression of either wild type or constitutively active forms of Gαq induced dilated cardiomyopathy [46], [47], whereas mice with cardiomyocyte-specific deletion of Gαq/Gα11 are resistant to ventricular hypertrophy induced by pressure overload [48]. This evidence concerns the gene GNAQ and dilated cardiomyopathy.