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Mice with targeted disruptions of SUR1 [7, 8] or the inward rectifying K + channel [9, 10] were still capable of secreting insulin in response to glucose stimulation, suggesting that GSIS does not solely operate through the K ATP channel

8), suggesting that rapamycin decreased the activation of STR CAR T cells to a greater extent than LTR CAR T cells and may explain the difference in mouse survival in the Nalm6 model