Again using the exon 1 floxed allele, mice were crossed with rat insulin promoter Cre recombinase line (to delete exon 1 in β-cells), or a glucagon promoter Cre (to delete in α cells), and the result was that the β-cell knockout mice showed many of the original features of the global knockout including glucose intolerance and a reduction in glucose stimulated insulin secretion, whilst in contrast, α cell deletion showed no abnormalities in plasma glucagon levels or glucose homeostasis [59•]. The gene discussed is INS; the disease is Glucose intolerance.