Moreover, IFN-α stimulation of PBMCs isolated from all groups of mice resulted in significant phosphorylation of AKT, IκB-α, STAT1, and STAT2; however, if we subtracted the normalized phosphorylation of these proteins without stimulation from their values upon IFN-α stimulation, this calculation revealed that type I IFN signaling during diabetes was clearly perturbed. The gene discussed is IFNA1; the disease is diabetes mellitus.