Upregulated Orai1 was reported to be a stress response molecule in cardiac hypertrophy, and Orai1 channel inhibition preserved left ventricular systolic function and promoted normal Ca2+ handling after pressure overload.[8] A regulatory role of SGK1 on the expression of Orai1/STIM1 was suggested by previous studies.[43, 44] Consistent with this, decreased calcium accumulation and Orail1/STIM1 were detected in HBT‐treated cardiomyocytes, suggesting that HBT‐mediated heart protection may be related to its regulation of calcium levels via inhibiting SGK1. This evidence concerns the gene STIM1 and cardiac hypertrophy.