ANKRD1 and cardiac hypertrophy: In mice, total Ankrd1 knockout or cardiac-restricted overexpression did not produce an abnormal phenotype [26], [33], which is in agreement with our finding that in vivo overexpression of Ankrd1 alone did not induce cardiac hypertrophy when no pathological stress was added, suggesting that Ankrd1 is redundant and plays pathological stress-dependent role.