Specifically, we investigated the extent of intracellular Ca2+ release; store-operated channels (SOC) mediated Ca2+ influx, particularly the contribution of the ICRAC channel to regulation of intracellular free Ca2+ in fibroblasts; the expression of the pore-forming ORAI1 and the store Ca2+ sensor, STIM1; magnitude of collagen secretion/deposition; and whether selective inhibition of the ICRAC channel could mitigate the altered collagen secretion/deposition, if any, in ventricular fibroblasts from HF patients. The gene discussed is ORAI1; the disease is hydrops fetalis.