Li et al. have also found that over-expressed Fbxo32 in neonatal rat cardiomyocytes disrupts the Akt-dependent pathway responsible for physiological cardiac hypertrophy.11 Interestingly, down-regulation of Fbxo32 in knockout mice produces the opposite effect, with the inhibition of cardiac hypertrophy in response to pressure overload [24], suggesting that there are different mechanisms by which FBXO32 induces atrophy and hypertrophy in cardiomyocytes [25]. This evidence concerns the gene FBXO32 and cardiac hypertrophy.