In association with the enhanced Ca2+ influx observed in lymphocytes isolated from UCD-T2DM rats, we also detected increased expression of Stim1—the ER Ca2+ sensor activated by store depletion—suggesting a compensatory mechanism driving Ca2+ entry in response to reduced ER Ca2+ levels This finding appears to parallel the D3M increase in SERCA 3 expression noted above, and may represent an induced mechanism pairing SERCA 3 and Stim1 upregulation to replenish Ca2+ stores. This evidence concerns the gene STIM1 and urea cycle disorder.