Following haemodynamic stress, deletion of SMIT1 significantly altered IP3/calcium effectors, including Carabin, which modulates cardiac hypertrophy through inhibition of the calcineurin/nuclear factor of activated T-cell and Ras/ERK1/2 pathways.<h4>Conclusion</h4>This work provides important insights into the role of myo-inositol and SMIT1 in cardiomyocytes. This evidence concerns the gene TBC1D10C and cardiac hypertrophy.