KMT2A and cardiac hypertrophy: In summary, while both models of Trx-1 depletion and overexpression of the non-functional Trx-1 protein demonstrate cardiac hypertrophy in response to Trx-1 disruption, the Trx-1 Myh6-Cre heart-specific knockout model exhibits more severe functional deficits, which is illustrated by the development of chronic heart failure and decreased lifespan.