Orai1 and STIM1 have been detected in rodents and human heart.4–6 Orai1/STIM1-mediated SOCE appears to be developmentally regulated in the heart, with prominent activity in developing cardiomyocytes7 and plays a role in maintaining ventricular diastolic Ca2+ homeostasis that is crucial for postnatal cardiac growth.4,8,9 However, while Orai1-deficient zebrafish developed spontaneous HF,5 global heterozygous Orai1+/- mice showed normal systolic function at baseline but developed more severe dilated cardiomyopathy after pressure overload insult.10 The gene discussed is ORAI1; the disease is hydrops fetalis.