It has been described that in cardiac hypertrophy, excessive trafficking of TRPC3 channels can lead to enhanced Ca2+ influx and stimulation of downstream signaling pathways like nuclear factor of activated T-cells (NFAT) and mammalian target of rapamycin (mTOR), leading to the development of hypertrophy (Brenner and Dolmetsch, 2007). This evidence concerns the gene MTOR and cardiac hypertrophy.