To this end, a recent study by Zheng et al. [163] demonstrated that in viral-infected macrophages or monocytes and samples from SLE patients and mouse models, AKT2 expression is decreased, and Akt2 deficiency promotes IFNβ1 and the production of ISGs to enhance an antiviral defense while heightening SLE in mouse models. The gene discussed is AKT2; the disease is systemic lupus erythematosus.