This effect has been attributed to PANDER amplifying glucagon signaling through hepatic cAMP and cAMP-response element-binding (CREB) protein, in contrast to the impaired Akt signaling that has been reported by Li et al. The observable and discernible phenotype within the PANKO-C57 model with regard to both fasting and fed glucose intolerance, which has not been seen in previous models, provides a measurable outcome and suitable metabolic end point to further investigate PANDER, and enables defined outcomes using this model that have not been observed in prior studies. The gene discussed is GCG; the disease is Glucose intolerance.