In direct contrast to both of the previous studies and to our findings highlighted above, Lee et al. reported that in a different genetic model of Cx3cr1 deficiency resulted in a defect in pancreatic insulin secretion[16] and, as a direct result the Cx3cr1-/- mice developed glucose intolerance and overt hyperglycemia on 60% high-fat diet. The gene discussed is CX3CR1; the disease is Hyperglycemia.