This may be because of an increased TRPC6 expression following TAC, as TRPC6 has been identified as a key player influencing the development of hypertrophy and heart disease by inducing calcineurin/NFAT signaling.36–38 Supportive of this concept, increased calcineurin activity after TAC was similar in WT and C-dnO1 mice suggesting that Orai1 is not instrumental in a calcineurin-dependent hypertrophic process in this pathology. This evidence concerns the gene TRPC6 and heart disorder.