Overexpressing active MEK7 in neonatal rat cardiomyocytes induced hypertrophy.70 However, an in vivo study showed that MEK7 overexpression in adult mice led to severe heart failure, which was due to the downregulation of Cx43 and the loss of gap junctions, and no obvious cardiac hypertrophy was observed.71 A loss-of-function study showed that delivery of a dominant-negative MEK4 expression vector to the heart blocked pressure overload-induced JNK activation and cardiac hypertrophy.72 Genetic deletion of MEKK1 attenuated cardiac hypertrophy induced by Gαq overexpression. This evidence concerns the gene MAP3K1 and heart failure.