AKT1 and Glucose intolerance: 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.