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. The gene discussed is SGK1; the disease is cardiac hypertrophy.